pituitrin and Hypertension--Renal

After several decades during which little attention was paid to vasopressin and/or urine concentration in clinical practice, interest in vasopressin has renewed with the availability of new, potent, orally active vasopressin-receptor antagonists--the vaptans--and with the results of epidemiological studies evaluating copeptin (a surrogate marker of vasopressin) in large population-based cohorts. Several experimental studies in rats and mice had previously shown that vasopressin, acting via vasopressin V2 antidiuretic receptors, contributes to the progression of chronic kidney disease; in particular, to autosomal dominant polycystic kidney disease. New epidemiological studies now suggest a role for vasopressin in the pathogenesis of diabetes mellitus and metabolic disorders via activation of hepatic V1a and/or pancreatic islet V1b receptors. The first part of this Review describes the adverse effects of vasopressin, as revealed by clinical and experimental studies in kidney diseases, hypertension, diabetes and the metabolic syndrome. The second part provides insights into vasopressin physiology and pathophysiology that may be relevant to the understanding of these adverse effects and that are linked to the excretion of concentrated nitrogen wastes and associated hyperfiltration. Collectively, the studies reviewed here suggest that more attention should be given to the vasopressin-thirst-urine concentration axis in clinical investigations and in patient care. Whether selective blockade of the different vasopressin receptors may provide therapeutic benefits beyond their present indication in hyponatraemia requires new clinical trials.

Topics: Animals; Benzazepines; Disease Progression; Humans; Hypertension, Renal; Incidence; Prevalence; Renal Insufficiency, Chronic; Tolvaptan; Vasopressins

Arterial hypertension and, less often, postural hypotension are frequently associated with diabetes mellitus, and with diabetic complications and death.. To review data on the relationship between hypertension and nephropathy in diabetes mellitus.. We reviewed data on both retinopathy and nephropathy in hypertensive diabetic patients. Data suggesting that vasopressin levels might affect blood pressure in upright patients with postural hypotension due to cardiocirculatory diabetic neuropathy were also examined. Antihypertensive treatment during different phases of diabetic nephropathy in insulin-dependent diabetes was reviewed.. The data showed that hydrochlorothiazide and nitrendipine reduce urinary protein excretion in parallel with a reduction in blood pressure. However, the decreases in urinary protein excretion induced by captopril are not correlated with a reduction in blood pressure and may be related to decreases in intraglomerular pressure found in patients with mild renal failure taking furosemide. Domperidone, a peripherally acting dopaminergic antagonist is an additional therapeutic option for the treatment of diabetic postural hypotension.

Topics: Antihypertensive Agents; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Diabetic Neuropathies; Diabetic Retinopathy; Female; Humans; Hypertension; Hypertension, Renal; Hypotension, Orthostatic; Male; Vasopressins

There are several mechanisms by which the central nervous system participates in the neural and humoral alterations associated with various forms of experimental hypertension. Structures in forebrain with multiple integrative roles in neuroendocrine control of the circulation are involved. Tissue surrounding the anteroventral region of the third cerebral ventricle (AV3V region) is involved physiologically in thirst, sodium homeostasis, osmoreception, secretion of vasopressin and natriuretic factor and sympathetic discharge to blood vessels. Destruction of this tissue prevents or reverses many forms of hypertension. In genetically based spontaneous hypertension, limbic structures such as the central nucleus of the amygdala rather than the AV3V region are the necessary neuroanatomic substrate. Recent evidence suggests that a circumventricular organ in brain stem, the area postrema, is also involved in the mediation of several forms of experimental hypertension. In renin- and nonrenin-dependent forms of renal hypertension, two major factors activate central mechanisms. First, direct central actions of angiotensin, acting through receptors in the subfornical organ and organum vasculosum of the lamina terminalis, increase sympathetic discharge and secretion of vasopressin through mechanisms integrated at the level of the AV3V region. Second, sensory systems originating in the kidney can activate increased sympathetic discharge through complex projection pathways involving forebrain systems. Mineralocorticoid hypertension appears to involve enhanced secretion of vasopressin and central vasopressinergic mechanisms also dependent on the AV3V region. Reciprocal connections between key central areas involved in control of arterial pressure provide the neuroanatomical basis for central nervous system participation in hypertension.

Topics: Blood Pressure; Central Nervous System; Humans; Hypertension; Hypertension, Renal; Mineralocorticoids; Vasopressins

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.

Topics: Acute Disease; Acute Kidney Injury; Animals; Central Nervous System Diseases; Desoxycorticosterone; Humans; Hypertension; Hypertension, Malignant; Hypertension, Renal; Hypertension, Renovascular; Kidney Failure, Chronic; Rats; Rats, Brattleboro; Rats, Inbred SHR; Vasopressins

Topics: Angiotensin II; Animals; Cardiac Output; Cardiomyopathies; Dogs; Hemodynamics; Homeostasis; Humans; Hypertension; Hypertension, Renal; Norepinephrine; Rabbits; Renal Artery Obstruction; Renin-Angiotensin System; Vascular Resistance; Vasopressins

Topics: Aldosterone; Angiotensin II; Biological Transport, Active; Bradykinin; Catecholamines; Estrogens; Glomerular Filtration Rate; Glucagon; Hormones; Humans; Hypertension, Renal; Kidney; Kidney Tubules, Distal; Kidney Tubules, Proximal; Loop of Henle; Mineralocorticoids; Natriuresis; Parathyroid Hormone; Potassium; Progesterone; Prostaglandins; Thyroid Hormones; Vasopressins; Water-Electrolyte Balance

Topics: Angiotensin II; Animals; Blood Pressure; Hypertension, Malignant; Hypertension, Renal; Hyponatremia; Juxtaglomerular Apparatus; Osmolar Concentration; Pepstatins; Plasma Volume; Rats; Renin; Saralasin; Vasopressins; Water-Electrolyte Imbalance

Topics: Benzothiadiazines; Body Water; Diabetes Insipidus; Diuretics; Humans; Hypernatremia; Hypertension, Renal; Hyponatremia; Hypothalamus; Infusions, Parenteral; Kidney Concentrating Ability; Osmotic Pressure; Pituitary Gland; Sodium; Sodium Chloride; Sodium Chloride Symporter Inhibitors; Vasopressins

Diagnostic approaches evolve steadily. Selective renal arteriography and determination of renal vein renins have replaced differential clearances and translumbar aortography. The hydrated intravenous pyelogram remains helpful in assessing physiologic significance and complements both aortography and renin determinations. Except for young patients, medical treatment rather than surgical management usually is preferred.

Topics: Adult; Creatinine; Dehydration; Female; Humans; Hydrogen-Ion Concentration; Hypertension, Renal; Kidney Function Tests; Middle Aged; Renal Artery Obstruction; Renin; Saline Solution, Hypertonic; Sodium; Sodium Chloride; Urography; Vasopressins; Water-Electrolyte Balance

Topics: Angiotensin II; Animals; Blood Pressure; Blood Proteins; Blood Vessels; Carotid Arteries; Cats; Dogs; Dose-Response Relationship, Drug; Drug Interactions; Epinephrine; Glucocorticoids; Guinea Pigs; Hindlimb; Hypertension; Hypertension, Renal; Kidney; Mineralocorticoids; Norepinephrine; Prostaglandins; Rabbits; Rats; Regional Blood Flow; Retinal Vessels; Saphenous Vein; Serotonin; Vasoconstrictor Agents; Vasopressins

Topics: Acidosis; Acute Kidney Injury; Alkalosis; Amyloidosis; Hodgkin Disease; Humans; Hyperkalemia; Hypernatremia; Hypertension, Renal; Hypokalemia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Multiple Myeloma; Neoplasms; Nephritis; Nephrotic Syndrome; Osmolar Concentration; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Angiotensin II; Animals; Catecholamines; Denervation; Dogs; Feedback; Hemorrhage; Hypertension, Renal; Hypertonic Solutions; Juxtaglomerular Apparatus; Kidney; Papaverine; Potassium Chloride; Receptors, Drug; Renal Artery; Renin; Sodium Chloride; Vasopressins

Topics: Adrenal Cortex Hormones; Animals; Biopsy; Body Weight; Diet, Sodium-Restricted; Eclampsia; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Nephritis; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pyelonephritis; Sodium; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Female; Humans; Hypertension, Renal; Kidney; Kidney Diseases; Norepinephrine; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Renin; Time Factors; Vasopressins

Topics: Acute Kidney Injury; Glomerulonephritis; Humans; Hypertension, Renal; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Kidneys, Artificial; Nephrotic Syndrome; Pyelonephritis; Transplantation, Homologous; Vasopressins

Assessment of plasma renin activity (PRA) in renal vein blood is used in the diagnosis of unilateral renovascular hypertension (URVH). Recently also other markers of renal ischaemia (atrial natriuretic peptide, adrenalin, nonadrenaline and dopamine) have been described. The present study aimed to assess renal handling of vasopressin (AVP) by the ischaemic kidney in patients with URVH. In 16 patients with URVH, PRA and AVP were estimated in renal vein blood of the ischemic (IK) and non-ischemic kidney (NK), in arterial blood (A) and in blood samples withdrawn from the inferior vena cava (VCI) below the orifices of the renal veins. In contrast to PRA no significant difference between plasma levels of AVP in renal vein blood of the ischaemic and non-ischaemic kidney was noticed (4.8 +/- 0.9 pg/ml vs 5.1 +/- 0.8 pg/ml respectively).. Chronic hypoperfusion of the kidney does not influence renal handling of AVP in patients with URVH. Thus assessment of AVP in renal vein blood in these patients is deprived of diagnostic value.

Topics: Adult; Biomarkers; Female; Humans; Hypertension, Renal; Ischemia; Kidney; Male; Middle Aged; Renal Artery Obstruction; Vasopressins

Congenital nephrogenic diabetes insipidus is a rare disorder in which the kidney is insensitive to the antidiuretic hormone, vasopressin. In most cases, a mutation in the vasopressin type 2(V2) receptor gene is the genetic cause of the disease. So far, few cases of congenital nephrogenic diabetes insipidus with hypertension have been reported. We report one male case of congenital nephrogenic diabetes insipidus accompanied by hypertension. The patient was a 24-year-old man who had suffered from polyuria and polydipsia since infancy and had been found to have hypertension at about 16 years. He was admitted to hospital in May 2000 for investigation of polyuria and hypertension with a high plasma level of renin activity of 10.4 ng/ml/hr. On physical examination, the blood pressure was 150/90 mmHg and the daily urinary output was 18.5 l. There was no change in urine volume and urine osmolality after an intramascular injection of vasopressin and water deprivation. The blood pressure and plasma renin activity were increased from 127/73 mmHg to 146/87 mmHg and from 4.9 ng/ml/hr to 6.1 ng/ml/hr, respectively, by a 4-hour dehydration test. He was found to have a C-to-T transition at nucleotide position 675 by sequencing analysis of the V2 receptor gene. After administration of hydrochlorothiazide, both the blood pressure and urine volume were reduced. Consequently, it was suggested that activation of the renin-angiotensin system by dehydration, at least in part, contributed to high blood pressure in this case.

Topics: Adult; Diabetes Insipidus, Nephrogenic; Humans; Hypertension, Renal; Male; Vasopressins

We analyzed the effects of a possible interaction between nitric oxide deficiency and mineralocorticoids on the long-term control of blood pressure and renal and endocrine variables. Six groups of uninephrectomized male Wistar rats were used: control animals and rats that received (1) N(G)-nitro-L-arginine methyl ester (L-NAME) subpressor (0.5 mg/100 mL drinking fluid), (2) L-NAME pressor (35 mg/100 mL drinking fluid), (3) deoxycorticosterone acetate (DOCA; 12. 5 mg/wk per rat), (4) DOCA plus L-NAME subpressor, or (5) L-NAME pressor plus DOCA. For all groups, the drinking fluid was tap water or 1% NaCl solution. We measured the time course of tail systolic blood pressure (SBP) and body weight for 3 weeks in all rats. At the end of the experimental period, we measured mean arterial pressure (direct recording) and endocrine and renal variables. Tail SBP rose significantly in the DOCA plus L-NAME subpressor-treated group but remained at normotensive levels in the DOCA-treated group. The addition of L-NAME to the subpressor dose accelerated the blood pressure increase in DOCA-salt hypertensive rats. The simultaneous administration of DOCA and L-NAME increased blood pressure and mortality rates in rats that drank water or saline compared with the rats treated with L-NAME alone. The subpressor dose of L-NAME did not increase blood pressure in saline-drinking rats. We conclude that impaired NO synthesis results in increased sensitivity to the pressor effect of mineralocorticoids in the presence or absence of an increased saline intake. Hence, nitric oxide contributes to the adaptative response to mineralocorticoid excess, perhaps through the facilitation of natriuresis and, thus, control of blood pressure.

Topics: Animals; Blood Pressure; Desoxycorticosterone; Drinking; Enzyme Inhibitors; Hypertension, Renal; Male; Mineralocorticoids; Natriuresis; NG-Nitroarginine Methyl Ester; Nitric Oxide; Rats; Rats, Wistar; Sodium Chloride; Vasopressins

The specific vasopressin V1 receptor agonist (V1AG; [Phe2,Ile3,Orn8]vasopressin) was infused (2.0 ng.kg-1.min-1) into the renal medullary interstitial space to determine the effects of selective medullary V1 receptor stimulation on sodium and water excretion in normal rats. Responses were compared with those of arginine vasopressin (AVP) and vasopressin V2 receptor stimulation resulting from infusion of a V1 receptor antagonist with AVP. Medullary infusion of V1AG or AVP in euvolemic rats produced no changes in hemodynamics or glomerular filtration rate. V1AG increased urine flow > 60% in euvolemic rats, whereas no change was observed with AVP. This response could not be explained by a rise of arterial pressure or by volume retention. With V2 stimulation in euvolemic rats, urine flow was decreased. In water diuretic rats, V1AG produced no change, whereas AVP infusion decreased urine flow. The results provide in vivo evidence that tubular V1 vasopressin receptor activity results in increased urine flow and thereby modulates the antidiuretic actions of vasopressin in the euvolemic state.

Topics: Animals; Arginine Vasopressin; Diuresis; Glomerular Filtration Rate; Hydrostatic Pressure; Hypertension, Renal; Kidney Medulla; Male; Natriuresis; Ornipressin; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Renal Circulation; Vasopressins

2-(N-Propyl-N[(2'-[1H-tetrazol-5-yl]biphenyl-4yl)methyl]amin o) pyridine-3-carboxylic acid (ABBOTT-81988), a novel nonpeptide angiotensin II (AII) antagonist, was evaluated to characterize its antihypertensive activity in the conscious renal hypertensive rat. Oral or i.v. administration of ABBOTT-81988 at 0.03 to 0.3 mg/kg produced a dose-dependent, sustained decrease in mean arterial pressure (MAP; control 162-173 mm Hg, n = 27) of approximately 20 to 70 mm Hg. At a dose of 0.3 mg/kg p.o., ABBOTT-81988 lowered MAP to a normotensive level for more than 24 hr and did not change heart rate. During its antihypertensive effect (delta MAP, -28% approximately -35%), ABBOTT-81988 (0.1-03 mg/kg i.v.) decreased total peripheral resistance (delta resistance, -31% approximately -43%), and cardiac output remained either unchanged or slightly elevated. ABBOTT-81988 (0.3 mg/kg i.v.) produced an additional antihypertensive effect (delta MAP, -12 +/- 2%, n = 5) in captopril-pretreated (10 mg/kg i.v.) hypertensive rats, but captopril (10 mg/kg i.v.) had no effect in ABBOTT-81988-pretreated (0.3 mg/kg i.v.) rats. In the normotensive rat, ABBOTT-81988 (0.3 mg/kg p.o.) had no effect on basal MAP, but it inhibited the AII-induced (0.1 microgram/kg i.v.) pressor response by 51% to 91% for 24 hr, whereas the responses to norepinephrine (0.3 microgram/kg i.v.), vasopressin (0.03 IU/kg i.v.) and bradykinin (3 micrograms/kg i.v.) were not affected. It is concluded that ABBOTT-81988 is a safe and efficacious AII antagonist that may have use in the treatment of human hypertension.

Topics: Angiotensin II; Animals; Antihypertensive Agents; Bradykinin; Electrocardiography; Hemodynamics; Hypertension, Renal; Male; Nicotinic Acids; Norepinephrine; Rats; Rats, Sprague-Dawley; Tetrazoles; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Cyclic AMP; Cyclic GMP; Diagnosis, Differential; Electrocardiography; Exercise Test; Humans; Hypertension; Hypertension, Renal; Male; Renin-Angiotensin System; Vasopressins

The administration of the antithyroid drug methimazole to rats via drinking water prevented the development of hypertension that usually accompanies subtotal nephrectomy and saline drinking (1% NaCl). In methimazole-treated rats, elevated blood pressure induced 5 weeks previously returned to normotensive levels. Pressor responsiveness to angiotensin, vasopressin and norepinephrine in unanesthetized rats was studied after prevention of hypertension in control, low-renal-mass hypertensive (LRM) and low-renal-mass methimazole-treated (LRM-M) rats, and in the reversion study in LRM and LRM-M rats. In LRM rats, responsiveness to vasoconstrictors was increased, whereas responsiveness to vasoconstriction was clearly reduced in LRM-M rats after prevention and reversion studies. These results suggest that (a) thyroid hormones are required in the early and established phases of LRM hypertension, and (b) the decreased pressor responsiveness to vasoconstrictors may play a role in the prevention and reversion of this type of hypertension following methimazole administration. However, the changes in pressor responsiveness may also be secondary to the reduction in blood pressure.

Topics: Administration, Oral; Angiotensin II; Animals; Blood Pressure; Heart Rate; Hypertension, Renal; Male; Methimazole; Norepinephrine; Rats; Rats, Inbred Strains; Vasoconstrictor Agents; Vasopressins

Renal water and electrolyte handling and related plasma hormone levels were measured in male and female New Zealand genetically hypertensive and normotensive rats, in an attempt to establish any potentially important sex-related differences in these parameters. Male hypertensive rats had higher blood pressure than female hypertensive rats, but normotensive rats showed no such sex difference. Both groups of males had higher fluid turnover rates than respective females, and this was associated with raised plasma vasopressin in hypertensive males. Female hypertensive rats excreted more sodium, potassium and chloride in association with lower plasma aldosterone and higher corticosterone levels compared with the other groups. Plasma electrolytes did not differ between the four groups, but plasma osmolality was higher in hypertensive than normotensive rats of both sexes. A higher rate of electrolyte loss and lower fluid turnover in association with reduced plasma vasopressin may contribute to the lower blood pressure of female compared with male hypertensive rats.

Topics: Aldosterone; Angiotensin II; Animals; Blood Pressure; Chlorides; Corticosterone; Female; Hypertension, Renal; Kidney; Male; Oxytocin; Potassium; Rats; Rats, Inbred SHR; Sex Characteristics; Sodium; Vasopressins; Water-Electrolyte Balance

1. Partial (5/6) renal ablation was performed in Long Evans rats treated with vehicle or a vasopressin V1-receptor antagonist, in control Long Evans rats, and in homozygous Brattleboro rats which lack endogenous vasopressin. 2. In control and vasopressin-blocked Long Evans rats, 3 weeks following partial renal ablation, systolic blood pressure was 215 +/- 5 and 199 +/- 9 mmHg and, urinary protein excretion was 54 +/- 4 and 50 +/- 3 mg day-1, respectively. 3. The pressor response to exogenous vasopressin was significantly (P less than 0.05) reduced in rats treated with the V1-receptor antagonist (ED50 mmHg 5.0 +/- 1.6 vs. 0.09 +/- 0.01 micrograms kg-1). 4. In control Long Evans and in Brattleboro rats, 3 weeks following renal ablation, systolic blood pressure was 204 +/- 10 and 191 +/- 7 mmHg, and urinary protein excretion was 97 +/- 27 and 71 +/- 5 mg day-1, respectively. 5. Histological examination of the remaining kidney tissue demonstrated significant glomerular hyalinization following renal ablation but no differences between any of the groups. 6. The data indicate that neither vasopressin nor the urinary concentrating mechanism is likely to be involved in the hypertension and proteinuria associated with partial renal ablation.

Topics: Animals; Blood Pressure; Body Weight; Hypertension, Renal; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Male; Osmolar Concentration; Proteinuria; Rats; Rats, Brattleboro; Urodynamics; Vasopressins

To assess the roles of vascular prostaglandins in the hypertension of chronic renal failure, the release of prostacyclin and thromboxane (TX) from aorta was evaluated in male Sprague-Dawley rats, the renal mass of which was reduced by removing one kidney and two-thirds of the contralateral kidney ("5/6 nephrectomy"). Five-sixths nephrectomy was followed by significant rises in serum creatinine to 0.55 +/- 0.03 mg/dl and urea nitrogen to 42.9 +/- 3.8 mg/dl, with a concomitant rise in mean blood pressure from 121.6 +/- 1.6 mmHg to 155.3 +/- 8.4 mmHg. In 5/6 nephrectomized rats, the release of TX A2 from aorta, as measured by its stable metabolite TX B2, increased by 60% (p less than 0.01) and prostacyclin, as measured by its stable metabolite 6-keto-prostaglandin, F1 alpha (6-keto-PG F1 alpha) increased by 51% (p less than 0.05). The amounts of both TX B2 and 6-keto-PG F1 alpha released from aorta were closely related to the height of mean blood pressure. These results suggest that the enhanced vasoconstrictor TX production in the vascular walls may be relevant to hypertension in rats with subtotal renal ablation. The adaptive increase in prostacyclin production in the vascular walls may compensate for the elevation of blood pressure due to chronic renal failure in this animal model.

Topics: Animals; Aorta; Blood Pressure; Body Weight; Epoprostenol; Hypertension, Renal; Kidney; Male; Nephrectomy; Rats; Rats, Inbred Strains; Thromboxanes; Vasoconstrictor Agents; Vasopressins

The authors present the indices of blood pressure (BP), plasma renin activity, the concentration of aldosterone, cortisol, adrenocorticotropic and antidiuretic hormones in 56 patients with arterial hypertension resulting from kidney parenchymatous diseases before hemosorption and at varying time after it. A decrease in the patients' BP is shown to occur in parallel with the redistribution of the blood levels of the above hormones. Possible mechanisms of BP reduction are discussed.

Topics: Adolescent; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Adult; Aldosterone; Blood Pressure; Female; Hemoperfusion; Humans; Hydrocortisone; Hypertension, Renal; Male; Middle Aged; Potassium; Renin; Sodium; Vasopressins

The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 +/- 0.6 pg/ml vs 0.8 +/- 0.1 in normal rat, P less than 0.05) but not to pressor levels. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1, receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Dose-Response Relationship, Drug; Ethylamines; Female; Hypertension, Renal; Kidney Medulla; Norepinephrine; Rats; Renin; Vasopressins

The hemodynamic changes associated with the onset of one-kidney, figure-8, renal-wrap hypertension were monitored in rats fed a high-sodium diet. In addition, the hemodynamic contributions of the sympathetic nervous system (SNS) and arginine vasopressin (AVP) were assessed during the 1st week of hypertension. Renal wrapping caused mean arterial pressure (MAP) to increase significantly from 108 +/- 4 to 140 +/- 4 mmHg on day 5 after renal surgery. The hypertension was associated with a significant bradycardia and no significant change in cardiac output (CO), as measured with an electromagnetic flow probe. Total peripheral resistance (TPR) was significantly elevated to 140% above control value on day 5 after renal surgery. Ganglionic blockade caused similar decreases in MAP and TPR in normotensive and hypertensive animals. Sympathetic blockade after pretreatment with a specific vascular antagonist of AVP, [1-beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin ([d(CH2)5Tyr(Me)]AVP), caused a greater depressor response in the renal-wrapped animals as compared with the effect of ganglionic blockade alone in these animals. The effect of [d(CH2)5Tyr(Me)]AVP alone on the hemodynamics was not different between the two groups of rats. After ganglionic blockade pretreatment, [d(CH2)5Tyr(Me)]AVP caused a significant decrease in MAP and TPR in the renal-wrapped animals. In addition, the difference in MAP and TPR between the two groups of rats was eliminated after combined blockade of AVP and the SNS. The results of this study indicated that the onset of hypertension was a result of an activation of neurohumoral mechanisms to increase TPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Hemodynamics; Hypertension, Renal; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Sodium; Sympathetic Nervous System; Vasopressins

One-kidney, figure-8 renal wrapped and sham-operated rats maintained on high sodium intake were studied to determine plasma concentrations of vasopressin during the onset of hypertension. Animals were chronically prepared with femoral artery and vein catheters. Arterial blood samples were taken from conscious rats before and 3 days after renal wrap or sham operation while donor blood was simultaneously infused intravenously. Three days after surgery, arterial pressure, plasma osmolality and plasma vasopressin concentration increased significantly in the renal wrapped animals and remained unchanged in the sham-operated rats. Ganglionic blockade with hexamethonium and atropine produced equivalent decreases in arterial pressure and increases in plasma vasopressin concentration in the two groups of rats. Subsequent administration of the V1 vasopressin antagonist, d(CH2)5Tyr(Me)AVP, caused a significantly greater fall in arterial pressure in the hypertensive rats. These results provide further evidence for a contribution of vasopressin to sodium-dependent hypertension.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Heart Rate; Hematocrit; Hypertension, Renal; Male; Osmolar Concentration; Potassium; Rats; Rats, Inbred Strains; Sodium; Vasopressins

The counter-regulatory effects in response to blood pressure reduction by propyldazine were studied in conscious dogs with bilateral cellophane perinephritis hypertension. During a 22-day period of chronic treatment, the initial increase in heart rate, plasma renin activity, angiotensin II, aldosterone, and vasopressin, which indicate counter-regulation to the drug induced decrease in blood pressure, vanished. On the fifth day of treatment another, presumably cellular mechanism, had taken over the restitution of blood pressure and thereby led to tolerance towards the action of further propyldazine administration. Seven days after the end of chronic treatment a renewed propyldazine administration did not produce the same effects as obtained with the first administration; after 28 days the hypotensive effect of propyldazine was identical to the one observed before treatment.

Topics: Animals; Antihypertensive Agents; Blood Pressure; Dogs; Drug Tolerance; Female; Hypertension, Renal; Pyridazines; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins

Topics: Humans; Hypertension, Renal; Kidney; Prostaglandins; Renin-Angiotensin System; Sodium; Vasopressins

There is evidence for an increased secretion of vasopressin in most models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension, one- and two-kidney renal hypertension, partial nephrectomy-salt hypertension, the spontaneously hypertensive rat (SHR), the Dahl salt-sensitive rat on a high-salt diet, and human essential hypertension. In most forms of hypertension, there is also an increased pressor responsiveness to vasopressin as well as to other pressor agents. Blockade of vasopressin with either a competitive antagonist or a specific antiserum lowered blood pressure substantially in DOC-salt hypertension, two-kidney, one-clip hypertension, the stroke-prone SHR with well-established hypertension, and the Dahl S rat treated with captopril. In rats with diabetes insipidus, one- and two-kidney renal hypertension, but not DOC-salt hypertension, can be produced. There is evidence that vasopressin can contribute to some models of hypertension as either a pressor or an antidiuretic agent.

Topics: Animals; Desoxycorticosterone; Disease Models, Animal; Humans; Hypertension; Hypertension, Renal; Hypertension, Renovascular; Nephrectomy; Rats; Rats, Inbred Strains; Rats, Mutant Strains; Species Specificity; Vasopressins

Topics: Aldosterone; Blood Pressure; Blood Volume; Captopril; Humans; Hypertension; Hypertension, Renal; Hypertension, Renovascular; Potassium; Proline; Renin; Renin-Angiotensin System; Sodium; Vasopressins; Water-Electrolyte Balance

Plasma arginine vasopressin (AVP) levels were elevated in both one-kidney, one-clip [1K-1C) and two-kidney, one-clip (2K-1C) hypertensive Long-Evans rats. Homozygous Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI), which are completely devoid of vasopressin, were made hypertensive using the 1K-1C Goldblatt models for renal hypertension. The 2K-1C DI rats developed hypertension at the same rate and to the same degree as normal 2K-1C hypertensive Long-Evans rats. The development of hypertension in 1K-1C DI rats was similar to the normal 1K-1C hypertensive Long-Evans rats. However, the absolute levels of systolic blood pressure reached were significantly less in the vasopressin-deficient rats. Treatment with 1-desamino-8-D-arginine vasopressin (DDAVP), the synthetic analogue of arginine vasopressin that has high antidiuretic but low pressor potencies, was associated with restoration of water balance in the volume-depleted DI rats and also restored blood pressure to hypertensive levels equivalent to the 1K-1C Long-Evans rats. These studies suggest that vasopressin is not essential for the development of experimental renal hypertension in rats but may contribute to the absolute levels of systolic blood pressure reached through its properties as an antidiuretic hormone.

Topics: Animals; Arginine Vasopressin; Diabetes Mellitus, Experimental; Hypertension, Renal; Osmolar Concentration; Pituitary Gland; Potassium; Rats; Rats, Inbred Strains; Sodium; Vasopressins

An attempt was made to produce one-clip, one-kidney hypertension in the rat with diabetes insipidus (DI). Renal artery constriction in unilaterally nephrectomized DI rats (DI-clip) resulted in an increased blood pressure in all 9 rats, but this response was only transient in 3 rats. The magnitude of the hypertension was less in the DI-clip rats than in Long-Evans rats subjected to the same protocol (LE-clip). Infusion of saralasin i.v. at doses of 10 and 30 micrograms/kg . min. 4 to 6 weeks after surgery was without effect on mean arterial pressure in LE-clip and control DI rats, but substantially lowered blood pressure in the DI-clip rats (p less that 0.05 - 0.01). It is concluded that vasopressin is not essential for the production of one-clip, one kidney hypertension in the rat, and that, in the DI rat, the renin-angiotensin system is an important factor in this form of hypertension.

Topics: Angiotensin II; Animals; Blood Pressure; Diabetes Insipidus; Disease Models, Animal; Dose-Response Relationship, Drug; Hypertension, Renal; Hypertension, Renovascular; Hypothalamic Diseases; Male; Muridae; Saralasin; Vasopressins; Water-Electrolyte Balance

The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension was investigated in the conscious dog. Intravenous infusion of synthetic arginine vasopressin to elevate plasma levels approximately fivefold to 31 pg/ml caused bradycardia in normal dogs, together with suppression of plasma renin activity and angiotensin II. This plasma level of vasopressin also caused elevation of mean arterial blood pressure in dogs with pharmacological total autonomic blockade. A similar degree of elevation of plasma vasopressin concentration was observed following mild nonhypotensive hemorrhage; more severe hemorrhage resulted in an approximate 100-fold increase in plasma vasopressin levels. Severe renal artery constriction in unilaterally nephrectomized dogs caused a marked rise in mean arterial blood pressure, but only a doubling of plasma vasopressin concentration. A suppressor infusion of vasopressin did not potentiate the pressor response to infused angiotensin II. It is concluded that vasopressin may play a role in normal cardiovascular homeostatic responses, but it is unlikely to have a significant direct vasoconstrictor role in the pathogenesis of this form of experimental renal hypertension.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Dogs; Heart Rate; Hypertension, Renal; Ischemia; Male; Renal Artery; Vasopressins

Topics: Abdominal Neoplasms; Angiotensin II; Blood Pressure; Child; Humans; Hypertension, Renal; Hypertension, Renovascular; Male; Nephrectomy; Pheochromocytoma; Saralasin; Vasopressins

1. After 4.5 months of renal hypertension in rats renal artery 'declipping' was performed. Eight weeks afterwards paired hindquarter perfusions were performed on the declipped rats and normotensive control rats, exploring the relationships between mean arterial pressure and flow, from maximal vasodilatation to maximal vasoconstriction, induced by graded noradrenaline infusions. Left ventricular weights were measured. 2. Declipping caused a fall in mean arterial pressure from 180 to 135 mmHg, though still after 8 weeks the mean pressure was 19% higher than in normotensive control rats. 3. All parameters reflecting design and reactivity of the resistance vessels and left ventricular weight decreased significantly, but not as much as mean arterial pressure, and were still significantly increased compared with those of control rats. 4. This neither mean arterial pressure nor cardiovascular design was normalized 8 weeks after 'reversal' of long-standing renal hypertension, in contrast to short-standing renal hypertension where both are completely normalized 3 weeks after declipping.

Topics: Animals; Barium; Blood Pressure; Cardiovascular System; Hypertension, Renal; Male; Norepinephrine; Rats; Renal Artery; Vascular Resistance; Vasopressins

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.

Topics: Animals; Autonomic Nervous System; Blood Pressure; Dehydration; Dogs; Hemorrhage; Hypertension, Renal; Hypertension, Renovascular; Male; Vasopressins

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Hypertension, Malignant; Hypertension, Renal; Immune Sera; Male; Natriuresis; Rats; Renal Artery Obstruction; Sodium; Vasoconstriction; Vasopressins; Water-Electrolyte Balance

Pressor reactivity to noradrenaline or vasopressin was studied in unanaesthetized, pithed and isolated perfused hindquarter, preparations from renal and spontaneously hypertensive rats. Unanaesthetized renal and spontaneously hypertensive rats showed hyperreactivity to noradrenaline and vasopressin. Vascular responses of noradrenaline in pithed and isolated perfused hindquarter preparations were to a lesser extent but significantly greater in the renal hypertensive rat, while responses of pithed and isolated perfused hindquarter preparations to noradrenaline were within normal limits in the spontaneously hypertensive rat.

Topics: Adrenalectomy; Animals; Hemodynamics; Hindlimb; Hydroxydopamines; Hypertension; Hypertension, Renal; Male; Norepinephrine; Rats; Sympathetic Nervous System; Vasopressins

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.

Topics: Acute Kidney Injury; Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Hypertension; Hypertension, Renal; Immune Sera; Injections, Intraventricular; Radioimmunoassay; Rats; Vasopressins

1. Blood pressure is controlled by both integrated neurogenic and humoral vasoactive mechanisms. 2. Both vasopressor (angiotensin and vasopressin) and vasodepressor (bradykinin) hormonal peptides have been identified. 3. In acute experimental renal hypertension in the rat plasma renin, angiotensin and vasopressin have all been shown to be elevated. 4. Associated with this increase in vasopressor hormonal peptides, urinary kallikrein excretion has been demonstrated to be reduced during the development of renal hypertension. 5. The level of blood pressure achieved in experimental renal hypertension is probably a summation of these vasoactive peptides as well as other factors.

Topics: Angiotensin II; Animals; Female; Hypertension, Renal; Kallikreins; Male; Peptides; Rats; Renin; Vasopressins

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.

Topics: Angiotensin II; Animals; Blood Pressure; Diet; Diet, Sodium-Restricted; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Models, Biological; Natriuresis; Paraneoplastic Endocrine Syndromes; Rats; Renin; Research; Sodium; Terminology as Topic; Vasopressins

The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling.

Topics: Animals; Corticosterone; Desoxycorticosterone; Hypertension, Renal; Kidney; Male; Potassium; Rats; Sodium; Vasopressins; Water; Water-Electrolyte Balance

Topics: Age Factors; Animals; Aorta, Thoracic; Barium Sulfate; Blood Pressure; Body Water; Body Weight; Cardiomegaly; Constriction; Dose-Response Relationship, Drug; Heart Ventricles; Hypertension, Renal; Kidney; Male; Muscle, Smooth; Norepinephrine; Organ Size; Renal Artery; Time Factors; Vasopressins

Topics: Animals; Aorta, Thoracic; Barium; Blood Pressure; Blood Vessels; Body Weight; Chlorides; Dose-Response Relationship, Drug; Female; Heart Rate; Heart Ventricles; Hemodynamics; Hypertension; Hypertension, Renal; Kidney; Male; Muscle, Smooth; Norepinephrine; Organ Size; Rats; Regional Blood Flow; Stimulation, Chemical; Vascular Resistance; Vasopressins

Topics: Aminohippuric Acids; Animals; Carbon Radioisotopes; Constriction; Female; Glomerular Filtration Rate; Hypertension, Renal; Inulin; Kidney; Kidney Concentrating Ability; Kidney Function Tests; Loop of Henle; Natriuresis; Osmolar Concentration; Potassium; Rats; Regional Blood Flow; Renal Artery Obstruction; Sodium; Urine; Vasopressins; Water

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.

Topics: Anesthesia, General; Angiotensin II; Animals; Arteries; Autonomic Nerve Block; Blood Pressure; Desoxycorticosterone; Diuretics; Furosemide; Hydrochlorothiazide; Hypertension; Hypertension, Renal; Male; Norepinephrine; Pentobarbital; Rats; Renin; Sodium Chloride; Tyramine; Vasoconstrictor Agents; Vasopressins

Topics: Angiotensin II; Animals; Aorta, Thoracic; Culture Techniques; Desoxycorticosterone; Disease Models, Animal; Hypertension; Hypertension, Renal; Male; Norepinephrine; Phenylephrine; Rabbits; Rats; Renin; Tyramine; Vasoconstrictor Agents; Vasopressins

Topics: Angiotensin II; Animals; Aorta, Thoracic; Biological Assay; Culture Techniques; Histamine H1 Antagonists; Hypertension, Renal; Norepinephrine; Phenylephrine; Rabbits; Rats; Receptors, Drug; Serotonin Antagonists; Tyramine; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Blood Pressure; Carbamates; Female; Ganglionic Stimulants; Guanethidine; Hypertension, Renal; Hypotension; Nicotine; Norepinephrine; Physostigmine; Piperazines; Pyrrolidines; Quaternary Ammonium Compounds; Rats; Tachyphylaxis; Tyramine; Vasopressins

Topics: Acetylcholine; Angiotensin II; Brachial Artery; Forearm; Humans; Hypertension, Renal; Norepinephrine; Regional Blood Flow; Tachyphylaxis; Vasopressins

Topics: Acute Disease; Aldosterone; Angiotensin II; Animals; Anuria; Dogs; Glomerular Filtration Rate; Hypertension, Renal; Kidney; Liver Cirrhosis; Male; Organ Size; Renal Veins; Renin; Sodium; Vasopressins

Topics: Angiotensin II; Animals; Blood Pressure; Female; Hypertension, Renal; Hypoxia; Kidney; Nephrectomy; Norepinephrine; Rats; Renin; Ureteral Obstruction; Vasopressins

Topics: Adolescent; Adult; Aminohippuric Acids; Contrast Media; Creatinine; Diuresis; Humans; Hyperplasia; Hypertension, Renal; Kidney Function Tests; Methods; Middle Aged; Renal Artery Obstruction; Sodium; Sodium Chloride; Urea; Urinary Catheterization; Urography; Vasopressins

Topics: Animals; Blood Pressure; Carotid Sinus; Diuresis; Dogs; Electric Stimulation; Glomerular Filtration Rate; Hypertension, Renal; Kidney; Natriuresis; Pituitary Gland, Posterior; Vasopressins

1. In the intact or nephrectomized rat, the pressor responses to synthetic angiotensin-II-amide, beta-angiotensin-II and native "rat angiotensin" could be inhibited by intravenous injection of rabbit serum containing antibodies against synthetic angiotensin-II-amide.2. The pressor responses to vasopressin or noradrenaline were not influenced by anti-angiotensin serum.3. A single injection of anti-angiotensin serum inhibited the pressor responses to angiotensin-II-amide for a period of 2.5 hr.4. Intravenous infusion or daily intraperitoneal injection of anti-angiotensin serum did not influence blood pressure levels in renal hypertensive rats.

Topics: Angiotensin II; Animals; Antibodies; Blood Pressure; Hypertension, Renal; Immune Sera; Injections; Nephrectomy; Norepinephrine; Pressoreceptors; Rabbits; Rats; Vasopressins

Topics: Adult; Aged; Cobalt Isotopes; Diuresis; Diuretics; Female; Glomerular Filtration Rate; Humans; Hypertension; Hypertension, Renal; Iodine Isotopes; Iodohippuric Acid; Kidney Function Tests; Male; Mannitol; Middle Aged; Pyelonephritis; Renal Artery Obstruction; Urea; Vasopressins; Vitamin B 12

Topics: Adolescent; Adult; Blood Volume; Dehydration; Diabetes Insipidus; Female; Hematocrit; Humans; Hyperaldosteronism; Hypertension, Renal; Male; Renin; Sodium; Vasopressins; Water

Topics: Angiotensin II; Animals; Blood Pressure; Blood Urea Nitrogen; Female; Hypertension, Renal; Kidney; Proteus Infections; Pyelonephritis; Rats; Renin; Streptococcal Infections; Vasopressins

Topics: Aldosterone; Animals; Hypertension, Renal; Kidney Function Tests; Rats; Renin; Tissue Extracts; Vasopressins

Topics: Angiotensin II; Animals; Hexamethonium Compounds; Hypertension; Hypertension, Renal; Male; Norepinephrine; Rats; Vasopressins

Topics: Angiotensin II; Blood Pressure; Diagnosis, Differential; Humans; Hypertension; Hypertension, Renal; Renal Artery Obstruction; Vasopressins

Topics: Animals; Biological Assay; Humans; Hypertension, Renal; Kidney Diseases; Kidney Function Tests; Plasma; Preoperative Care; Rats; Renal Artery Obstruction; Renal Veins; Vascular Surgical Procedures; Vasopressins

Topics: Blood Pressure Determination; Diagnosis; Diuresis; Glomerular Filtration Rate; Humans; Hypertension; Hypertension, Renal; Insulin; Kidney; Kidney Diseases; Kidney Function Tests; Natriuresis; Pharmacology; Renal Artery Obstruction; Urea; Vasopressins

Topics: Angiotensins; Arginine Vasopressin; Diuresis; Electrolytes; Fluids and Secretions; Hypertension, Renal; Hypertension, Renovascular; Kidney; Natriuresis; Pharmacology; Physiology; Potassium; Rats; Research; Urinary Catheterization; Urine; Vasopressins

Topics: Humans; Hypertension, Renal; Kidney Diseases; Kidney Function Tests; Osmosis; Urine; Vasopressins

Topics: Aldosterone; Angiotensins; Animals; Blood Pressure; Corticosterone; Desoxycorticosterone; Female; Hypertension; Hypertension, Renal; Kidney; Norepinephrine; Pregnancy; Pregnancy, Animal; Rats; Renin; Research; Vasopressins

Topics: Bis-Trimethylammonium Compounds; Epinephrine; Hypertension; Hypertension, Renal; Pharmacology; Rabbits; Renal Artery Obstruction; Research; Vasomotor System; Vasopressins

Topics: Blood Pressure; Body Weight; Diuresis; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Inulin; Kidney; Kidney Function Tests; Nephrosclerosis; Osmolar Concentration; Pathology; Pharmacology; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Vasopressins

Topics: Angiotensins; Arteriosclerosis; Hypertension; Hypertension, Renal; Kidney; Skin Tests; Vasopressins

Topics: Animals; Hypertension; Hypertension, Renal; Rats; Vasopressins