pituitrin and Uremia

Physiologic data provided evidence for specific urea transporter proteins in red blood cells and kidney inner medulla. During the past decade, molecular approaches resulted in the cloning of several urea transporter cDNA isoforms derived from two gene families: UT-A and UT-B. Polyclonal antibodies were generated to the cloned urea transporter proteins, and their use in integrative animal studies resulted in several novel findings, including: (1) UT-B is the Kidd blood group antigen; (2) UT-B is also expressed in many non-renal tissues and endothelial cells; (3) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (4) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; and (5) UT-A protein abundance is increased in uremia in both liver and heart. This review will summarize the knowledge gained from studying molecular mechanisms of urea transport and from integrative studies into urea transporter protein regulation.

Topics: Angiotensins; Animals; Biological Transport, Active; Cell Membrane Permeability; Diabetes Mellitus; Homeostasis; Humans; Kidney; Kidney Concentrating Ability; Kidney Medulla; Membrane Transport Proteins; Mice; Rats; Renal Insufficiency; Urea; Urea Transporters; Uremia; Urine; Vasopressins

Topics: Absorption; Adaptation, Physiological; Animals; Body Water; In Vitro Techniques; Kidney Tubules; Kidney Tubules, Collecting; Kidney Tubules, Proximal; Phosphates; Potassium; Rabbits; Uremia; Vasopressins

Topics: Acidosis, Renal Tubular; Aldosterone; Ascites; Diuretics; Hepatic Encephalopathy; Humans; Hypokalemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules, Distal; Liver Cirrhosis; Liver Transplantation; Sodium; Transplantation, Homologous; Uremia; Vasopressins; Water-Electrolyte Imbalance

Topics: Aging; Angiotensin II; Animals; Atropine; Bartter Syndrome; Bone and Bones; Carbohydrate Metabolism; Cardiovascular Diseases; Drug Hypersensitivity; Gastric Mucosa; Gastrointestinal Diseases; Heart; Hematologic Diseases; Humans; Kidney Failure, Chronic; Parathyroid Diseases; Parathyroid Hormone; Pharmaceutical Preparations; Rabbits; Rats; Thyroid Diseases; Uremia; Vasopressins; Vitamin D

Topics: Alcoholism; Aldosterone; Animals; Diuretics; Dogs; Humans; Kidney; Kidney Failure, Chronic; Magnesium; Magnesium Deficiency; Parathyroid Hormone; Rats; Uremia; Vasopressins

Endothelial dysfunction is a key initiating event in vascular disease in chronic kidney disease (CKD) patients and haemodialysis (HD) patients exhibit significant vascular abnormalities. To understand this further, we examined how ex vivo intrinsic function in isolated arteries correlates with in vivo assessments of cardiovascular status in HD patients. Abdominal fat biopsies were obtained from 11 HD patients and 26 non-uremic controls. Subcutaneous arteries were dissected and mounted on a wire myograph, and cumulative concentration-response curves to noradrenalin, endothelin-1, a thromboxane A2 agonist (U46619), angiotensin II, vasopressin, bradykinin (BK), acetylcholine (ACh) and sodium nitroprusside (SNP) were constructed. Pulse wave velocity and blood pressure were measured in HD patients. Enhanced (P<0.05-0.0001) maximal contractile responses (Rmax) to all spasmogens (particularly vasopressin) were observed in arteries from HD patients compared to controls, and this effect was more pronounced in arteries with an internal diameter>600 µm. The potency (pEC50) of U46619 (P<0.01) and vasopressin (P<0.001) was also increased in arteries>600 µm of HD patients. The maximal relaxant response to the endothelium-dependent dilators ACh and BK were lower in HD patients (P<0.01-P<0.0001) (worse for ACh than BK); however the endothelium-independent dilator SNP was similar in both groups. PWV was significantly correlated with the vasoconstrictor response to vasopressin (P = 0.042) in HD patients. HD patients are primed for hypertension and end organ demand ischaemia by a highly sensitised pressor response. The failure of arterial relaxation is mediated by endothelial dysfunction. Intrinsic vascular abnormalities may be important in sensitising HD patients to recurrent cumulative ischaemic end organ injury.

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Acetylcholine; Aged; Angiotensin II; Arteries; Bradykinin; Endothelin-1; Female; Humans; Kidney; Male; Middle Aged; Muscle Contraction; Muscle Relaxation; Myography; Nitroprusside; Norepinephrine; Pulse Wave Analysis; Renal Dialysis; Uremia; Vasoconstrictor Agents; Vasopressins

Adrenocortical steroid hormones are importantly involved in the regulation of extracellular fluid volume. The present study was aimed at examining whether aldosterone and/or glucocorticoid regulates the abundance of aquaporin-3 (AQP3), -2, and -1 in rat kidney. In protocol 1, rats were adrenalectomized, followed by aldosterone replacement, dexamethasone replacement, or combined aldosterone and dexamethasone replacement (rats had free access to water but received a fixed amount of food). Protocol 2 was identical to protocol 1, except that all groups received fixed daily food and water intake. In both protocols 1 and 2, aldosterone deficiency was associated with increased fractional Na excretion and severe hyperkalemia. Semiquantitative immunoblotting revealed that aldosterone deficiency was associated with a dramatic downregulation of AQP3 abundance. Consistent with this, immunocytochemistry and immunoelectron microscopy revealed a marked decrease in AQP3 labeling in the basolateral plasma membranes of collecting duct principal cells. In contrast, AQP1 and AQP2 abundance and distribution were unchanged. Glucocorticoid deficiency revealed no changes in AQP3, -2, or -1 abundance. In protocol 3, Na restriction (to increase endogenous aldosterone levels) or exogenous aldosterone infusion in either normal rats or vasopressin-deficient Brattleboro rats was associated with a major increase in AQP3 abundance. In protocol 4, aldosterone levels were clamped by infusion of aldosterone, while Na intake was altered from a low to a high level. Under these circumstances, there were no changes in AQP3 or AQP2 abundance, although the level of the thiazide-sensitive Na-Cl cotransporter was decreased. In conclusion, the results uniformly demonstrate that aldosterone regulates AQP3 abundance independently of Na intake. In contrast, changes in glucocorticoid levels in these models do not influence AQP3 or AQP2 abundance. Therefore, in the collecting duct aldosterone may regulate, at least in part, AQP3 expression in addition to regulating Na and K transport.

Topics: Adrenalectomy; Aldosterone; Animals; Aquaporin 3; Aquaporins; Deficiency Diseases; Glucocorticoids; Kidney Tubules, Collecting; Male; Microscopy, Immunoelectron; Mineralocorticoids; Natriuresis; Nitrogen; Potassium; Rats; Rats, Inbred Strains; Urea; Uremia; Vasopressins; Water

Hemodialysis influences the transport of water through the erythrocytic membrane, and induces morphologic and functional modifications. Recently water channels, called aquaporins (AQP), have been identified on the membrane of red blood cells. The aim of the present study was, therefore, to evaluate any relationships between volumetric changes in erythrocytes (MCV), plasma osmolarity and membrane expression of AQP1 in 22 uremic patients during a hemodialysis session, and compare value with those in a control group of 22 healthy volunteers. Membranal AQP1 expression was evaluated using three methods: indirect immunofluorescence under confocal microscopy, immunoenzymatic method after membrane extraction, and immunoblotting. In uremic subjects, at baseline membrane AQP1 expression was significantly lower, whereas plasma osmolality was higher than in controls. At 1 and 2 h of replacement therapy, a progressive increase was observed in erythrocytic AQP1, values similar to those in controls being attained after 3.5 h. During the session osmolality values reduced progressively, becoming significantly lower than basal values. The mean erythrocytic corpuscular volume in patients with ESRD was significantly lower than in cntrols at baseline. This value increased during hemodialysis, attaining statistical significance with respect to the basal value at 3.5 h of dialysis. Close correlations were found between plasma osmolality and AQP1 values (r = -0.930; p < 0.05), and also between MCV and plasma osmolality trend (r = -0.909; p < 0.05). There was a linear correlation (r = 0.63, p < 0.05) between plasma AVP concentrations and plasma osmolality. The variations found in plasma osmolarity during hemodialysis, may induce AQP1 expression on the membrane of intact red blood cells.

Topics: Adult; Aged; Aquaporin 1; Aquaporins; Blood Group Antigens; Blood Pressure; Erythrocyte Indices; Erythrocytes; Female; Hemoglobins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Osmolar Concentration; Potassium; Renal Dialysis; Sodium; Uremia; Vasopressins

We have previously shown that a chronic reduction in plasma vasopressin level slowed the progression of chronic renal failure (CRF) in Sprague Dawley rats. The aim of the present study was to determine the respective contribution of pressor (V1) and antidiuretic (V2) effects of vasopressin on progression. Male homozygous Brattleboro rats with hereditary central diabetes insipidus were submitted to 5/6 nephrectomy. They were divided into three groups, two of which received chronic i.p. infusion of AVP (V1 + V2 effects) or dDAVP (V2 effects). The third group served as control (CONT). The doses of AVP and dDAVP were chosen so as to produce urine osmolality similar to that observed in 5/6 Nx Sprague Dawley rats. All rats ate the same amount of food and drank water ad libitum. Renal function was studied for 13 weeks. All three groups showed a marked hypertension. Rats infused with dDAVP, but not those infused with AVP, had a higher creatininemia, anemia and urinary protein excretion than CONT rats. In the dDAVP but not the AVP group, fractional excretion of urea was markedly decreased and plasma urea concentration rose much more than that of creatinine. These results show that V2 but not V1 effects play a major role in the deleterious influence of vasopressin on progression, at least in Brattleboro rats. The more severe progression seen in dDAVP rats could indirectly result from the V2-mediated effects on the collecting duct resulting in a decreased efficiency of urea excretion, an increased intrarenal urea recycling, and a rise in plasma urea concentration. Both the toxic effects of urea and the recently demonstrated V2-mediated increase in glomerular hemodynamics might be involved in the deleterious influence of V2 agonism.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Body Weight; Creatinine; Diabetes Insipidus; Disease Models, Animal; Disease Progression; Kidney; Kidney Failure, Chronic; Male; Proteinuria; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; Uremia; Vasopressins

Ultrafiltration during haemodialysis (HD) may be the cause of blood pressure (BP) decline due to reduction of blood volume. In some patients, however, BP does not decrease or even rises during HD. The aim of the study was to answer the question: do uraemic hypertensive patients, showing a decline of mean blood pressure (MAP) during HD session (group A) differ from those showing a stable MAP during HD session (group B) with respect to hormonal profile of aldosterone (ALD), vasopressin (AVP), atrial natriuretic peptide (ANP), endothelin-1,2 (ET-1,2), blood nitric oxide (NO) and plasma renin activity (PRA). A total of 39 haemodialysed, hypertensive patients (17 female, 22 men) were studied. 24 patients (group A) showed a MAP decline of 10 mm Hg or more, while 15 patients (group B) showed MAP changes of less than +/- 10 mm Hg during HD session. PRA, ALD, AVP, ANP, ET-1,2, NO concentration were assessed in blood samples withdrawn from the arterial blood line before HD and after 60, 120, 180 and 240 minutes of HD session. Plasma ET-1,2 and blood NO concentration were also assessed after 30 minutes of HD. BV was continuously monitored with a Crit-Line equipment, BP was measured before and every 30 minutes on HD. Before HD session both examined groups showed similar baseline plasma levels of ALD, AVP, ANP, ET-1,2, NO, PRA and MAP. A 4-hours HD induced a significant increase in plasma ALD and AVP concentrations and a significant decline in ANP level in both groups of patients. In group A, PRA and blood NO concentration increased significantly, while plasma ET-1,2, level did not change during HD. In group B, no significant changes in PRA and blood NO level were noticed, while plasma ET-1,2 rose markedly. In addition in group B, a significant positive correlation was found between MAP and plasma ET-1,2 level changes, but a significant negative correlation between MAP and blood NO level changes.. Patients with a decline of MAP over 10 mm Hg during HD differ from those with a stable MAP by a different response of plasma ET and blood NO to HD induced volume changes.

Topics: Aldosterone; Atrial Natriuretic Factor; Blood Volume; Female; Humans; Hypertension; Male; Nitric Oxide; Renal Dialysis; Severity of Illness Index; Uremia; Vasopressins

alpha-Human atrial natriuretic peptide (ANP) concentrations were measured in 11 diabetic patients with uremia and in 16 nondiabetic uremic controls undergoing renal transplantation after preanesthetic volume expansion with 1000 ml saline solution within 10 min. Two diabetic and seven nondiabetic patients received grafts from living donors and the rest from cadaveric donors. Volume expansion induced a significant increase in the cardiac filling pressures (P less than 0.001), which were kept at that level especially at declamping, which was preceded by mannitol infusion. The baseline mixed venous ANP levels were significantly higher in the diabetic (252 +/- 6 pg/ml) than in the nondiabetic group (103 +/- 14 pg/ml; P less than 0.05). In the nondiabetic group, ANP increased to 177 +/- 40 pg/ml as a response to volume loading (P less than 0.05); it was not clearly changed in the diabetic group. Arterial ANP increased from 267 +/- 55 to 343 +/- 75 pg/ml in the diabetic group (P less than 0.05 and from 102 +/- 17 to 147 +/- 31 pg/ml in the nondiabetic group (P less than 0.05). During transplantation, mixed venous ANP decreased to 125 +/- 55 pg/ml in the diabetic and to 80 +/- 10 pg/ml in the nondiabetic group (P less than 0.001). About 30% of circulating ANP was taken up by the transplant irrespective of postoperative graft function. Two patients in each group showed delayed diuresis requiring postoperative dialysis therapy (22% of all cadaveric transplantations). ANP levels at declamping had no correlation to the outcome of kidney function.

Topics: Adult; Atrial Natriuretic Factor; Blood Volume; Diabetic Nephropathies; Female; Humans; Kidney Transplantation; Lactates; Lactic Acid; Male; Renin; Uremia; Vasopressins

Bleeding time is prolonged following resection of kidney tissue as well as after ureteral occlusion. Bilateral nephrectomy raises bleeding time from 17 to 67 min, and blood loss can be increased from 2 to 12 microliters/min. Plasmatic coagulation factors remain unchanged in uremic rats. There is no influence of various surgical interventions producing uremia on function of thrombocytes. In rats with intact kidney function and following bilateral nephrectomy a diminution of bleeding time is demonstrable after administration of histamine or captopril. Shortening of bleeding time by the antifibrinolytic substance p-aminomethylbenzoic acid seems to indicate an increased fibrinolytic activity in uremic rats.

Topics: 4-Aminobenzoic Acid; Angiotensin II; Animals; Bleeding Time; Blood Coagulation; Captopril; Chlorisondamine; Enalapril; Female; Fibronectins; Histamine; Nephrectomy; para-Aminobenzoates; Platelet Aggregation; Rats; Rats, Inbred Strains; Uremia; Ureteral Obstruction; Vasopressins

In 5 haemodialyzed patients the influence of 3 months' erythropoietin (EPO) treatment on plasma renin activity (PRA), aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) was studied. Results were compared with those obtained in 7 uraemic patients showing a similar haematocrit value as patients after EPO therapy and with those obtained in 10 healthy subjects. EPO treatment did not influence significantly blood pressure but was suppressing PRA and plasma Ald levels, and raising plasma ANP concentrations. EPO treatment was without influence on AVP plasma levels. Data obtained in this study suggest that EPO-induced endocrine alterations are not due to increased blood volume and only partially related to improvement of uraemic anaemia.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Blood Pressure; Creatinine; Erythropoietin; Hematocrit; Homeostasis; Hormones; Humans; Male; Middle Aged; Renal Dialysis; Renin; Uremia; Vasopressins

Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age-matched control subjects (23.3 +/- 2.1 ml/min and 49.6 +/- 2.6 ml/min per 1.73 m2, P less than 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free-water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P less than 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P less than 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free-water reabsorption. Renal prostaglandin E2 may participate in the pathogenesis of azotemia by altering recycling of urea in the medulla.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Blood Urea Nitrogen; Dinoprostone; Female; Glomerular Filtration Rate; Humans; Kidney Concentrating Ability; Kidney Tubules; Male; Middle Aged; Prostaglandins E; Renin; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Blood; Humans; Kidney Failure, Chronic; Metabolic Clearance Rate; Polyuria; Renin-Angiotensin System; Ultrafiltration; Uremia; Vasopressins

Topics: Adrenocorticotropic Hormone; Aldosterone; Angiotensins; Carbohydrate Metabolism; Catecholamines; Endocrine System Diseases; Erythropoietin; Female; Gastrins; Gonadal Steroid Hormones; Humans; Hydrocortisone; Kidney Failure, Chronic; Male; Renal Dialysis; Renin; Thyroid Gland; Uremia; Vasopressins

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

Topics: Blood; Dehydration; Diabetic Coma; Glucagon; Humans; Hyperglycemia; Hyperglycemic Hyperosmolar Nonketotic Coma; Insulin; Kinetics; Osmolar Concentration; Sodium; Uremia; Vasopressins

The effect of inhibition of angiotensin II synthesis by captopril on the response of plasma ADH to the osmotic and volume-dependent stimuli has been studied in 15 uremic patients. Captopril administration had no effect either on basal plasma ADH or on plasma ADH response to the osmotic stimulus. Time-course of plasma ADH following hypertonic saline administration and sensitivity of the response (increase of plasma ADH related to increase of plasma sodium) were not modified. On the contrary, the response of plasma ADH to the volume-dependent stimulus induced by hemofiltration was markedly blunted by captopril administration. The sensitivity estimated from the slope of the regression line relating plasma ADH to the cumulated lost volume was clearly diminished. These results suggest that angiotensin II mediates ADH response only to the volume-dependent stimulus.

Topics: Adult; Aged; Angiotensin II; Blood; Captopril; Female; Humans; Male; Middle Aged; Osmolar Concentration; Sodium; Time Factors; Ultrafiltration; Uremia; Vasopressins

Topics: Acute Kidney Injury; Animals; Blood Volume; Ischemia; Kidney; Nephrectomy; Rats; Uremia; Vasopressins

Resistance of the chronically diseased kidney to vasopressin has been proposed as a possible explanation for the urinary concentrating defect of uremia. The present studies examined the water permeability and adenylate cyclase responsiveness of isolated cortical collecting tubules (CCT) from remnant kidneys of uremic rabbits to vasopressin. In the absence of vasopressin the CCTs of both normal and uremic rabbits were impermeable to water. At the same osmotic gradient, addition of a supramaximal concentration of vasopressin to the peritubular bathing medium led to a significantly lower net water flux per unit length (and per unit luminal surface area) in uremic CCTs than in normal CCTs. Transepithelial osmotic water permeability coefficient, P(f), was 0.0232 +/-0.0043 cm/s in normal CCTs and 0.0059+/-0.001 cm/s in uremic CCTs (P < 0.001). The impaired vasopressin responsiveness of the uremic CCTs was observed whether normal or uremic serum was present in the bath. Basal adenylate cyclase activity per microgram protein was comparable in normal and uremic CCTs. Stimulation by NaF led to equivalent levels of activity in both, whereas vasopressin-stimulated activity was 50% lower in the uremic than in the normal CCTs (P < 0.025). The cyclic AMP analogue, 8-bromo cyclic AMP, produced an increase in the P(f) of normal CCTs closely comparable to that observed with vasopressin. In contrast, the P(f) of uremic CCTs was only minimally increased by this analogue and was not further stimulated by theophylline. These studies demonstrate an impaired responsiveness of the uremic CCT to vasopressin. This functional defect appears to be a result, at least in part, of a blunted responsiveness of adenylate cyclase to vasopressin. The data further suggest that an additional defect in the cellular response to vasopressin may exist, involving a step (or steps) subsequent to the formation of cyclic AMP.A unifying concept of the urinary concentrating defect of uremia is proposed which incorporates a number of hitherto unexplained observations on the concentrating and diluting functions of the diseased kidney.

Topics: Adenylyl Cyclases; Animals; Body Water; Cyclic AMP; Female; In Vitro Techniques; Kidney; Kidney Concentrating Ability; Nephrons; Perfusion; Permeability; Rabbits; Uremia; Vasopressins

Topics: Animals; Body Composition; Body Water; Dogs; Humans; Mathematics; Parenteral Nutrition; Potassium; Potassium Deficiency; Radioisotope Dilution Technique; Regression Analysis; Sepsis; Sodium; Sodium Isotopes; Starvation; Surgical Procedures, Operative; Tritium; Uremia; Vasopressins

Topics: Aged; Angiography; Anuria; Diabetes Insipidus; Diatrizoate; Female; Glucose; Humans; Kidney; Kidney Cortex; Kidney Medulla; Mannitol; Osmolar Concentration; Uremia; Urine; Vasopressins

Topics: Acute Disease; Adult; Amino Acids; Chlorides; Extracellular Space; Female; Humans; Hypokalemia; Hyponatremia; Levulinic Acids; Male; Nitrogen; Porphobilinogen; Porphyrias; Porphyrins; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Electroencephalography; Hormones, Ectopic; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Metabolic Diseases; Penicillins; Uremia; Vasopressins

Topics: Adult; Aged; Anemia, Hemolytic; Anemia, Hypochromic; Anemia, Sideroblastic; Aspirin; Blood Urea Nitrogen; Creatinine; Diagnosis, Differential; Female; Hematuria; Humans; Kidney Failure, Chronic; Male; Middle Aged; Phenacetin; Pyelonephritis; Radioisotope Renography; Scotland; Substance-Related Disorders; Uremia; Urinary Tract Infections; Urine; Urography; Vasopressins

Topics: Adolescent; Child; Child, Preschool; Cystinosis; Diabetes Insipidus; Diuresis; Glomerulonephritis; Humans; Hydronephrosis; Infant; Infant, Newborn; Kidney Diseases; Kidney Diseases, Cystic; Polyuria; Pyelonephritis; Uremia; Vasopressins

Topics: Animals; Dogs; Glomerular Filtration Rate; Kidney; Pressure; Reflex; Urea; Uremia; Urinary Bladder; Urinary Bladder Neck Obstruction; Urination; Vasopressins

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Anuria; Glucose Tolerance Test; Humans; Middle Aged; Peritoneal Dialysis; Uremia; Vasopressins

Topics: Acute Kidney Injury; Atropine; Biomedical Research; Blood Volume; Convalescence; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Edema; Epinephrine; Female; Heart Failure; Hemorrhage; Humans; Hypertonic Solutions; Menstruation; Pharmacology; Placebos; Pregnancy; Renal Insufficiency; Salivation; Sweating; Uremia; Vasopressins; Water-Electrolyte Balance