pituitrin and Hypertension--Renovascular

In the last decade, our knowledge of the renal kallikrein-kinin system has been advanced significantly. More specific and sensitive methods for assessing its activity have been developed. Further, it has been found that in the kidney this system is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Data indicate that the kallikrein-kinin system interacts with other renal hormonal systems such as the prostaglandin and renin-angiotension-kinin system may participate in the control of renal function and the pathophysiology of renal diseases. An increase in kallikrein excretion has been observed after administration of antihypertensive drugs. The kallikrein-kinin system may therefore participate in their mechanism(s) of action. Our current knowledge suggests that the renal kallikrein-kinin system is an integral part of the intrarenal hormonal system that controls water and electrolyte excretion and participates in the regulation of blood pressure.

Topics: Animals; Dinoprostone; Humans; Hypertension, Renovascular; Kallikreins; Kidney; Kidney Diseases; Kinins; Nephrons; Peptidyl-Dipeptidase A; Prostaglandins E; Rats; Subcellular Fractions; Tissue Distribution; Vasopressins

The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.

Topics: Acute Disease; Angiotensin II; Animals; Arterial Occlusive Diseases; Central Nervous System; Chronic Disease; Disease Models, Animal; Dogs; Hemodynamics; Hypertension, Renovascular; Kidney; Ouabain; Perfusion; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasoconstriction; 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

One of the medicinal plants widely used by the population in the treatment of hypertension, atherosclerosis and circulatory disorders is Cuphea carthagenensis (Jacq.) J.F. Macbr. (Lythraceae), popularly known as 'sete sangrias', being found in Brazil, Hawaii and in South Pacific Islands. Despite the widespread use of this species by the population, its long-term antihypertensive and cardioprotective activities have not yet been scientifically evaluated.. To evaluate the possible cardioprotective effects of an ethanol-soluble fraction obtained from C. carthagenensis (ESCC) using ovariectomized hypertensive rats to simulate a broad part of the female population over 50 years of age affected by hypertension. In addition, the molecular mechanism that may be responsible for its cardiorenal protective effects was also explored.. Female Wistar rats were submitted to surgical procedures of bilateral ovariectomy and induction of renovascular hypertension (two-kidneys, one-clip model). The sham-operated group was used as negative control. ESCC was obtained and a detailed phytochemical investigation about its main secondary metabolites was performed. ESCC was orally administered at doses of 30, 100 and 300  mg/kg, daily, for 28 days, 5 weeks after surgery. Enalapril (15  mg/kg) was used as standard antihypertensive drug. Renal function was evaluated on days 1, 7, 14, 21 and 28. At the end of the experimental period, systolic, diastolic, mean arterial pressure and heart rate were recorded. The activity of the tissue enzymatic antioxidant system, thiobarbituric acid reactive substances, nitrotyrosine, nitrite, aldosterone and vasopressin levels, in addition to the activity of the angiotensin-converting enzyme were also evaluated. Additionally, vascular reactivity to acetylcholine, sodium nitroprusside, and phenylephrine, and the role of nitric oxide, prostaglandins, and K. ESCC-treatment induced an important cardiorenal protective response, preserving renal function and preventing elevation of blood pressure and heart rate in ovariectomized hypertensive rats. In addition, prolonged treatment with ESCC recovered mesenteric vascular reactivity at all doses used. This effect was associated with an important modulation of the antioxidant defense system with a possible increase in NO bioavailability. Additionally, NO/cGMP activation and K. A 28-days ESCC treatment reduces the progression of the cardiorenal disease in ovariectomized hypertensive rats. These effects seem to be involved with an attenuation of oxidative and nitrosative stress, affecting endothelial nitric oxide production and K

Topics: Aldosterone; Animals; Antihypertensive Agents; Blood Pressure; Cuphea; Cyclic GMP; Endothelium, Vascular; Female; Hypertension, Renovascular; Nitric Oxide; Nitrites; Nitrosative Stress; Oxidation-Reduction; Oxidative Stress; Peptidyl-Dipeptidase A; Phytochemicals; Plant Extracts; Plants, Medicinal; Potassium Channels; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances; Tyrosine; Vasodilator Agents; Vasopressins

Despite the importance of brain-mediated sympathetic activation in the morbidity and mortality of patients with high blood pressure, the precise cellular mechanisms involved remain largely unknown. We show that an imbalanced interaction between two opposing currents mediated by potassium (I(A)) and calcium (I(T)) channels occurs in sympathetic-related hypothalamic neurons in hypertensive rats. We show that this imbalance contributes to enhanced membrane excitability and firing activity in this neuronal population. Knowledge of how these opposing ion channels interact in normal and disease states increases our understanding of underlying brain mechanisms contributing to the high blood pressure condition.

Topics: 4-Aminopyridine; Action Potentials; Animals; Calcium Channel Blockers; Calcium Channels, T-Type; Calcium Signaling; Dendrites; Electrophysiological Phenomena; Gene Expression; Hypertension, Renovascular; Hypothalamus; Male; Medulla Oblongata; Membrane Potentials; Neurons; Nickel; Oxytocin; Paraventricular Hypothalamic Nucleus; Patch-Clamp Techniques; Rats; Rats, Wistar; Shal Potassium Channels; Sympathetic Nervous System; Vasopressins

10 patients with renovascular hypertension (HRV) and 12 healthy persons were examined under water immersion (WI) conditions without and after blockade of opioid receptors with 2 mg of naloxone. Blood pressure, body mass, change of plasma volume, plasma molality, PRA, and serum values of AVP, aldosterone and catecholamines were evaluated. There were no significant changes between the two examined groups before and after WI. It seems that the drop in blood pressure induced by WI is not only the result of diminished activation of RAAS. The role of opioid receptors in controlling blood pressure and other evaluated parameters is likely in both examined groups.

Topics: Adult; Aldosterone; Body Height; Body Weight; Case-Control Studies; Catecholamines; Female; Humans; Hypertension, Renovascular; Immersion; Male; Naloxone; Narcotic Antagonists; Osmolar Concentration; Plasma Volume; Renin-Angiotensin System; Vasopressins

Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.

Topics: Animals; Blood Pressure; Body Weight; Deamino Arginine Vasopressin; Desoxycorticosterone; Erythrocytes; Female; Hypertension, Renovascular; Ion Transport; Osmolar Concentration; Potassium; Rats; Rats, Brattleboro; Sodium; Vasopressins

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. In response to acute environmental stress (air jet), the borderline hypertensive rat exhibits a diuretic response, whereas the parental strains exhibit an antidiuretic response (spontaneously hypertensive rat) or no change in urine flow rate (Wistar-Kyoto rat). This study sought to investigate the role of the periventricular tissue surrounding the anteroventral third ventricle and vasopressin release in the diuretic response of the borderline hypertensive rat to acute environmental stress. Sixteen-week-old borderline hypertensive rats who had consumed a 1% NaCl diet for 10-12 weeks were given either electrolytic lesions of the anteroventral portion of the third ventricle or sham lesions. When exposed to acute environmental stress 4 weeks later, the increase in volume of dilute urine seen in the sham-lesion rats was not observed in the lesion rats. Plasma vasopressin concentration was decreased by acute environmental stress in the sham-lesion rats (15.2 +/- 4.0 to 10.9 +/- 1.7 pg/ml, p less than 0.05) but was unchanged in the lesion rats (12.3 +/- 2.0 to 13.4 +/- 4.0 pg/ml). In a separate group of intact borderline hypertensive rats, a constant intravenous infusion of vasopressin prevented the diuretic response to acute environmental stress. The results suggest that acute environmental stress produces a diuresis in the borderline hypertensive rats via a decrease in plasma vasopressin concentration that is dependent on the integrity of the periventricular tissue of the anteroventral portion of the third ventricle.

Topics: Animals; Blood Pressure; Female; Hemodynamics; Hypertension, Renovascular; Kidney; Male; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Stress, Mechanical; Sympathectomy; Sympathetic Nervous System; Vasopressins; Ventricular Function

Urinary digoxin-like factor, ADH, sodium and potassium excretion and urine osmolality were studied during the development of two pathogenically different models of hypertension, DOCA-salt (low-renin) and Gold-blatt 2 kidney-1 clip (renin-dependent). Urinary digoxin-like factor was increased in rats that were given saline (NaCl 1%) to drink, uninephrectomized-salt and DOCA-salt rats, with no significant differences between the two groups urinary ADH was elevated in DOCA-salt rats during the study, compared with uninephrectomized-salt rats. Urinary digoxin-like factor and urinary ADH were not significantly modified in Goldblatt 2 kidney-1 clip and sham-operated rats. In addition, positive correlations between digoxin-like factor urinary excretion and urinary ADH and also with sodium urinary excretion were found. These data suggest that: a) digoxin-like factor and ADH could play a role in the pathogenesis of DOCA-salt but not in Goldblatt 2 kidney-1 clip hypertension. b) A common mechanism may stimulate ADH and digoxin-like factor simultaneously. c) Digoxin-like factor plays a role in the control of urinary sodium excretion.

Topics: Animals; Blood Pressure; Desoxycorticosterone; Hypertension; Hypertension, Renovascular; Male; Natriuretic Agents; Potassium; Rats; Rats, Inbred Strains; Renin; Sodium; Vasopressins

We studied the possible contribution of increased vascular reactivity in the chronic phase of Goldblatt two kidney-one clip hypertension. Vascular reactivity was evaluated in aortic strips from hypertensive rats (16 weeks after inducing hypertension) and age-matched control rats. The findings were: a) increased sensitivity to vasopressin in the aortic tissue of hypertensive rats, b) a similar response to angiotensin II, noradrenaline and KCl in hypertensive and control rats, and c) reduced maximal response to angiotensin II compared with other vasoconstrictors in both groups of rats. These results suggest a possible role for vasopressin in the chronic phase of this model of hypertension.

Topics: Angiotensin II; Animals; Hypertension, Renovascular; In Vitro Techniques; Male; Muscle Contraction; Muscle, Smooth, Vascular; Norepinephrine; Potassium Chloride; Rats; Rats, Inbred Strains; Vasopressins

Blood flow in the superior mesenteric artery was observed with a chronically implanted electromagnetic flow probe in two-kidney, one-clip renovascular hypertensive rats (2K1C), one-kidney, one-clip renovascular hypertensive rats (1K1C), and normotensive control rats (NCR) in the conscious state. Arterial pressure was recorded with an indwelling catheter. Superior mesenteric resistance was calculated as arterial pressure divided by superior mesenteric flow. In all three groups of rats, superior mesenteric resistance remained almost unchanged when arterial pressure decreased markedly on ganglionic blockade with hexamethonium bromide. However, subsequent injection of a vasopressin antagonist (Manning compound) decreased superior mesenteric resistance significantly in 2K1C but not in 1K1C and NCR. Injection of vasopressin antagonist alone was without effect on arterial pressure and superior mesenteric flow in the three rat groups. Only 2K1C were judged to have appreciable sympathetic tone in resistance vessels of the superior mesenteric area, which was blocked by hexamethonium but compensated for by secondarily secreted vasopressin.

Topics: Animals; Blood Pressure; Hexamethonium Compounds; Hypertension, Renovascular; Male; Mesenteric Arteries; Rats; Rats, Inbred Strains; Regional Blood Flow; Sympathetic Nervous System; Vascular Resistance; Vasopressins

In rats with streptozotocin-induced diabetes an increase in arterial blood pressure was observed as early as the first week after the drug was injected. Blood pressure reached maximal values around the fourth week and remained stable for a long period of follow-up. The responsiveness of these rats to the three major vasopressor hormones, angiotensin II, norepinephrine, and vasopressin, was decreased in the early phase of diabetes and returned to normal in the late phase. Acute treatment at the third, sixth, and twelfth weeks with blockers of these vasopressor hormones resulted in a significant fall in blood pressure at the third week with captopril and at the twelfth week with propranolol plus phentolamine. No significant fall was observed when a specific vasopressin inhibitor was administered. Good control of the blood pressure was obtained when these rats were treated chronically with captopril or prazosin, and partial control was achieved when they were fed a low salt diet. An attenuation in arterial blood pressure levels was observed in rats with two-kidney, one clip hypertension when diabetes was induced by streptozotocin. Plasma creatine levels in diabetic rats were significantly higher than those in control rats only in the sixth and twelfth weeks. Electron microscopy revealed some minor glomerular lesions only at the twelfth week.

Topics: Angiotensin II; Animals; Blood Pressure; Captopril; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Humans; Hypertension; Hypertension, Renovascular; Kidney; Norepinephrine; Prazosin; Rats; Time Factors; Vasopressins

We have investigated the role of angiotensin II in the development of high blood pressure and in the maintenance of renal function during 2 weeks of one-kidney renal artery stenosis in conscious dogs. Responses to a fixed degree of inflation of a balloon cuff around the renal artery were compared in dogs with or without continuous enalapril (MK 421) treatment. In six untreated dogs, mean aortic pressure was increased by 17.1 +/- 2.0 mm Hg, due primarily to increases in total peripheral resistance with little change in cardiac output, while glomerular filtration rate, renal blood flow, renal artery pressure, and plasma renin activity were back to prestenosis levels. In seven enalapril-treated dogs mean aortic pressure was increased by 23.0 +/- 2.7 mm Hg and was not significantly different from that occurring in untreated dogs. This rise was due to increases in total peripheral resistance (10%) and cardiac output (12%). In the absence of angiotensin II, glomerular filtration rate remained low, at only 56 +/- 6% of prestenosis levels. Renal blood flow returned to normal, but the renal artery pressure remained 25% lower than control values. Thus, the main role of angiotensin II in chronic one-kidney Goldblatt hypertension does not appear to be through its pressor properties but rather through its actions in the kidney to preserve glomerular filtration. This effect on renal function persisted throughout the course of the hypertension, even when the plasma renin levels returned to normal.

Topics: Angiotensin II; Animals; Blood Pressure; Cardiac Output; Dogs; Enalapril; Glomerular Filtration Rate; Hypertension, Renovascular; Kidney; Male; Renal Artery; Renal Artery Obstruction; Renin; Vascular Resistance; Vasopressins; Water-Electrolyte Balance

There is evidence that neither activation of the renin-angiotensin system nor changes in sodium balance can fully explain the maintenance of blood pressure in Goldblatt hypertension. Thus, in Goldblatt two-kidney, one clip hypertension in the rat sodium balance is negative and in hypertension of a few months' duration plasma renin initially elevated has returned to normal. When hypertension is reversed by removal of the constricting clip from the renal artery, blood pressure falls within a matter of hours even when hypertension has been present for many months, suggesting that the effect of structural changes in vascular resistance vessels has been overcome. In addition, blockade of the renin-angiotensin system during renal artery declipping does not influence the pattern of the blood pressure fall. We investigated the role of the renomedullary vasodepressor system by inducing medullary necrosis with 2-bromo-ethylamine hydrobromide. This causes a moderate blood pressure increase in normal rats, and partly inhibits the fall of blood pressure in Goldblatt two-kidney, one clip hypertension when the renal clip is removed. Chemical medullectomy is associated with a slightly negative sodium balance, plasma volume contraction, a reduction in plasma renin activity and urinary PGE2, and a minimal elevation in plasma vasopressin. Blood pressure elevation appears to be attributable to inhibition of a vasodepressor system based on the renal medulla. Chemical medullectomy offers a valuable tool for investigating the role of this medullary vasodepressor system.

Topics: Animals; Dinoprostone; Disease Models, Animal; Hypertension, Renovascular; Kidney Medulla; Prostaglandins E; Rats; Renin; Renin-Angiotensin System; Sodium; Vasopressins

The effect of ketanserin (KET), a specific 5-hydroxytryptamine2 (5-HT2) receptor blockade, on pressor response to vasoactive substances was examined in rats with one-kidney, one clip renal artery stenosis of 2 days' duration (2-day clipped rat) and in rabbits with renal artery stenosis of 3 days' duration (3-day clipped rabbits). The 2-day clipped rats showed hyperresponsiveness to norepinephrine (NE), arginine vasopressin (AVP) and 5-HT. All hyperresponsiveness were attenuated by a subdepressor dose of KET. The infusion of KET, 10 micrograms/kg/min for 30 minutes, decreased mean arterial pressure of the 3-day clipped rabbits; the dose did not alter blood pressure of the normal controls. Exaggerated pressor response to NE was observed in the 3-day clipped rabbits and was abolished by a subdepressor dose of KET, 2.5 micrograms/kg/min. These results suggest that 5-HT may be involved in the enhanced pressor response to vasoconstrictor substances in the 2-day clipped rats and 3-day clipped rabbits, and that it may also play an important role in maintaining blood pressure in the 3-day clipped rabbits.

Topics: Animals; Hypertension, Renovascular; Ketanserin; Male; Norepinephrine; Rabbits; Rats; Renin; Vasopressins

The role of vasopressin (VP) in maintaining blood pressure in malignant two-kidney one-clip Goldblatt hypertension in chronically catheterized conscious rats was investigated by studying the effect of two structurally different VP pressor antagonists. Injections of either 20 micrograms/kg of dPTyr(Me)AVP or 10 micrograms/kg of d(CH2)5Tyr(Me)AVP failed to alter mean arterial pressure or heart rate, although both antagonists completely inhibited the pressor response elicited by exogenous VP. These results suggest, that VP is not involved as a pressor hormone in the maintenance of high blood pressure in this type of experimental hypertension.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Female; Hypertension, Malignant; Hypertension, Renovascular; Rats; Vasopressins

Topics: Animals; Arginine Vasopressin; Blood Pressure; Desoxycorticosterone; Hypertension; Hypertension, Renovascular; Male; Rats; Rats, Inbred Strains; Sodium; Spinal Cord; 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

The renal microcirculation was assessed in non-clipped kidneys of 23 Munich-Wistar rats with two-kidney one-clip Goldblatt hypertension. Four weeks after placement of a renal arterial clip, mean systemic arterial pressure averaged 163 +/- 5 mm Hg in hypertensive rats as compared to 108 +/- 2 in sham-operated controls (n = 6 rats). Non-clipped kidneys in hypertensive rats were characterized by higher glomerular capillary hydraulic pressures, single nephron glomerular filtration rate, and afferent arteriolar resistance. The glomerular capillary ultrafiltration coefficient was significantly reduced in hypertensive rats. In 10 of these rats, intravenous infusion of the angiotensin antagonist, saralasin, or the converting enzyme inhibitor, SQ20881, led to significant reductions in systemic arterial pressure and in afferent and efferent arteriolar resistance, on average by 8 +/- 3%, 15 +/- 4%, 28 +/- 5%, respectively. These changes were associated with significant increase in glomerular plasma flow, while ultrafiltration coefficient remained unaffected. In the presence of saralasin or SQ20881, infusion of a specific antagonist of the vascular action of arginine vasopressin led to significant systemic but not renal vasodilation. Thus, whereas systemic arterial pressure fell further, on average by 23 +/- 2%, renal arteriolar resistance remained constant, resulting in marked reduction in glomerular capillary hydraulic pressures (by 18 +/- 2%) and glomerular plasma flow rate (by 28 +/- 10%). Because of these pronounced reductions in glomerular pressures and flows induced by vasopressin antagonist, single nephron glomerular filtration rate fell markedly in hypertensive rats (by 34 +/- 6%) despite normalization of ultrafiltration coefficient. When hypertensive rats (n = 7) were treated with vasopressin antagonist alone, a modest fall in systemic arterial pressure was again observed in the absence of changes in renal arteriolar resistance. Due to this selective extrarenal vasodilatory action of vasopressin antagonist, glomerular capillary hydraulic pressure, plasma flow rate, and single nephron glomerular filtration rate again fell markedly. When these vasopressin antagonist pre-treated hypertensive rats were given saralasin or SQ20881, marked reductions in renal arteriolar resistance were observed in association with a significant increase in glomerular plasma flow rate. These observations made during acute inhibition of angiotensin II and vasopressin indicate that b

Topics: Angiotensin II; Animals; Blood Pressure; Glomerular Filtration Rate; Hypertension, Renovascular; Male; Microcirculation; Rats; Renal Circulation; Saralasin; Teprotide; Vasodilation; 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

Topics: Animals; Arginine Vasopressin; Autonomic Nervous System; Blood Pressure; Brain; Cardiac Output; Feedback; Hemodynamics; Humans; Hypertension; Hypertension, Renovascular; Models, Neurological; Pressoreceptors; Reflex; Spinal Cord; Vascular Resistance; 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

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

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