Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antihypertensive action of angiotensin-converting enzyme (ACE) inhibitors may be related to inhibition of systemic and local vascular angiotensin-II formation, to a potentiation of the local vascular kinin system with secondary stimulation of prostacyclin synthesis, and also to their effects on the central nervous system as well as on renal hemodynamics and excretory function. More detailed studies in patients with severe hypertension, previously not adequately controlled by conventional therapy with a diuretic, a beta-blocking agent and a vasodilator dihydralazine, showed that addition of the ACE inhibitor ramipril normalized systolic and diastolic blood pressure (BP) without hypotensive episodes or reflex tachycardia. ACE inhibition caused a change in the baroreceptor set point as we had previously demonstrated in healthy subjects, but baroreceptor sensitivity was not affected and the pressure response to exogenous norepinephrine remained unchanged by ACE inhibition. Despite the significant reduction in BP in our patients, endogenous creatinine clearance remained unaltered. Furthermore, the decrease in BP is accompanied by an initial natriuresis probably contributing to the BP-lowering effect of ACE inhibitors. Decreased proximal tubular reabsorption may include enhanced urate clearance reflected by a decrease in serum urate concentration which we observed despite continuous diuretic treatment. ACE inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. In our patients this resulted in a 10% decrease in urinary potassium excretion and a small rise in serum potassium concentration. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydroosmotic effect of vasopressin, thus resulting in a rise in free-water clearance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin-converting enzyme inhibition in patients with essential hypertension. 225 20

The rate of urine formation and its composition are influenced by the different drugs used during surgery. Anaesthetics act on renal function, not only directly, but also by producing changes in cardiovascular function and in neuroendocrine activity. Many factors may be incriminated: lowered blood pressure and cardiac output, increased sympathetic outflow (renal nerve stimulation and increased plasma catecholamines), increased release of renin, angiotensin and vasopressin. The effects of anaesthetics on the kidney go beyond a simple change in basal haemodynamics and include, for some drugs, an alteration in the ability for the kidney to autoregulate its blood flow and glomerular filtration rate. Studies on toad bladders showed a decrease in transport of water, sodium and organic anions. But, in fact, renal effects of anaesthetics in man and animals depend on the species, the anaesthetic and the method used to study the effect. Most barbiturates and inhalational anaesthetics tend to decrease renal blood flow (RBF) and glomerular filtration rate (GFR). These trends are gradually reversed during recovery. The effects of ketamine and diazepam are not clearly defined. Morphine and fentanyl decrease urine flow and GFR, whilst RBF increases or decreases, depending on whether a direct or indirect measurement technique was used. Muscle relaxants have little effect on renal function. Spinal and epidural anaesthesia only slightly decrease GFR and RBF in proportion to the decrease in mean arterial pressure. Obviously, the preexisting intravascular volume and the quantity of intravenous fluids given strongly influence the renal response to spinal and epidural anaesthesia. Some studies have shown that urine flow rate, creatinine clearance, urinary sodium excretion and RBF are reduced during mechanical ventilation with positive end-expiratory pressure. Surgery itself influences renal function by inducing alterations in prerenal haemodynamics. Operative stress leads to an increase in circulating catecholamines and angiotensin. Significant fluid shifts, excessive blood loss and redistribution of a third space may lead to a prerenal oliguric state, increasing secretion of vasopressin. Acute renal failure (ARF) is a frequently lethal complication of critical surgical illness, due to a variety of factors which interfere with glomerular filtration and tubular reabsorption, such as renal hypoperfusion or nephrotoxic insults. In fact, the initiating aggression ultimately culminates in the development of one or more of the maintenance factors (decreased tubular function, tubular obstruction, decreased GFR and RBF) that reduce urine flow and osmolar excretion. Good management during the perioperative period tends to minimize the risk of developing ARF.
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PMID:[Changes in renal function induced by anesthesia]. 227 18

Ten patients with amyotrophic lateral sclerosis were treated during 5 consecutive days with intravenous infusion of high-dose human leukocyte interferon-alpha (IFN-alpha) or placebo in a single-blinded randomized trial. To assess the effect of IFN on the water and electrolyte balance, serum electrolytes, creatinine, and antidiuretic hormone as well as urine excretion of electrolytes, aldosterone, and cortisol were measured before the trial and during the fourth day of IFN infusion. Compared with placebo the results showed a significant reduction of the mean serum calcium level (from 2.28 +/- 0.03 mmole/liter to 2.01 +/- 0.06 mmole/liter; p less than 0.01), that of the mean serum osmolality (from 296 +/- 9.9 mosm/kgH2O to 281 +/- 2.5 mosm/kgH2O; p less than 0.05) and that of the mean urinary excretion of magnesium (from 5.32 +/- 2.04 mmoles/liter to 2.65 +/- 1.68 mmoles/liter; p less than 0.05). Careful observation of water and electrolyte balance is emphasized during high-dose IFN treatment.
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PMID:Disturbance of the water and electrolyte balance during high-dose interferon treatment. 234 51

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.
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PMID:Hyponatremia and hypouricemia: differentiation from SIADH. 235 Sep 4

Lithium salts are widely used agents for the prophylactic treatment of affective disorders. Lithium salts may be associated with distal nephron dysfunction. Kallikrein is a protease which is generated by the distal nephron. We used an amidolytic assay of chromatographically purified enzyme to determine the urinary excretion rate of active kallikrein in relation to lithium treatment. All plasma lithium concentrations were within the therapeutic range (0.4 to 0.9 mmol/liter). In 15 patients the urinary excretion rate of active kallikrein was 267.4 +/- 65.6 mU/24 hrs before lithium treatment, and fell to 117.8 +/- 39.6 mU/24 hrs (P less than 0.05) on day 14 of lithium treatment. This reduction was associated with a decrease of immunoreactive kallikrein in the same urines by 66%. In another 15 patients who had undergone lithium therapy for an average period of 5.6 years, the urinary excretion rate of active kallikrein was 86.1 +/- 14.5 mU/24 hrs, while 21 age-matched healthy controls had an excretion rate of 364.1 +/- 58.4 mU/24 hrs (P less than 0.05). Measurements of immunoreactive kallikrein in the same urine samples demonstrated a reduction of kallikrein after long-term lithium treatment by 78%. These observations could not be attributed to changes in creatinine clearance, renal sodium or potassium excretion rates or plasma concentrations of aldosterone and vasopressin. Addition of lithium to the urine in vitro had no demonstrable effect on kallikrein measurement by amidolytic assay. We conclude that lithium in therapeutic plasma concentrations may directly suppress the secretion of kallikrein by renal connecting tubule cells.
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PMID:Lithium treatment reduces the renal kallikrein excretion rate. 238 81

A conclusion on relationships of the septum with both the antidiuretic and antinatriuretic systems in the regulation of the aqueous-electrolytic balance and renal function has been drawn as a result of the study of the drinking behaviour and renal reaction after the destruction of the lateral septal nucleus (LSN). This conclusion is based on the revealed increase in the urinary excretion of sodium, osmotically active substances, creatinine, titrating acids and ammonia after the LSN destruction. Moreover, an increase of the vasopressin level in the blood plasma, a decrease of aldosterone concentration as well as an activation of the drinking behaviour are noted.
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PMID:[Effect of destruction of the lateral septal nucleus on renal function]. 239 49

Serial measurements of urinary arginine vasopressin (AVP) were made in six severely birth asphyxiated newborn infants. In five infants serial plasma concentrations were also evaluated. There was a strong negative correlation between plasma AVP and plasma osmolality in these infants (r = -0.52, P = 0.0012). In neither the individual babies nor the group as a whole was there a significant correlation between plasma AVP and the urinary excretion of AVP even if the latter was standardised for creatinine content. Normal development at follow up was only observed in two asphyxiated infants who had consistently low urinary arginine vasopressin levels in the first days of life. Infants with consistently high urinary vasopressin concentrations either died or were severely abnormal in their subsequent development.
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PMID:The vasopressin response to severe birth asphyxia. 239 13

Vasopressin is the primary physiological factor regulating renal water reabsorption in mammals. Inhibitors of vasopressin-stimulated water reabsorption have previously been used as water diuretic agents in both experimental animals and man. The present studies describe and characterize the pharmacological effects of the potent vasopressin antagonist desGly d(CH2)5D-Tyr(Et)VAVP (SK&F 101926) and related analogs on renal water and solute excretion in conscious rats. Administration of SK&F 101926 was associated with dose-dependent increases in renal water excretion in conscious hydropenic rats. A selective vasopressin pressor (V1) antagonist (SK&F 100273) was inactive as a diuretic agent in these tests. SK&F 101926 antagonized, in a competitive fashion, exogenous vasopressin-stimulated antidiuresis in conscious water-loaded rats. Only modest increases in renal excretion of Na+, K+, and urea were observed when SK&F 101926 was administered. No changes in endogenous creatinine excretion were associated with the administration of SK&F 101926, suggesting that this drug does not affect glomerular filtration rate. The rank order of bioequivalency of alternative routes of administration of SK&F 101926 was intraperitoneal = intravenous = intramuscular = subcutaneous greater than intranasal much greater than rectal, ocular, and oral. SK&F 101926 (20 micrograms/kg/day) was effective in blocking the development of hyponatremia in a rat model of the syndrome of inappropriate antidiuretic hormone (SIADH). SK&F 100273 (100 micrograms/kg) hastened the onset of endotoxin-associated shock in rats. We conclude that SK&F 101926 is a potent water diuretic (aquaretic) agent in rats. The mechanism of action is most probably antagonism of vasopressin at renal epithelial (V2) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Discovery and therapeutic utility of vasopressin antagonists in rats. 243 70

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.
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PMID:Vasopressin in hyponatremia: what stimuli? 243 81

The effects of incremental exogenous alpha-human atrial natriuretic factor (ANF) infusion (10 and 25 ng.kg-1. min-1) on the cardiovascular, renal, and hormonal systems were examined in 22 healthy males. Successive 45-min infusions of ANF increased plasma levels five- and ninefold from a basal 42 +/- 5 pg/ml (P less than 0.01 and P less than 0.001). Hemodynamic responses provoked by ANF consisted solely of progressive reductions in central venous pressure (CVP) (P less than 0.05). Heart rate and mean arterial pressure were unaltered. Plasma renin activity, aldosterone, and vasopressin were not modified by either dose of ANF. However, plasma norepinephrine increased 32% during the 10-ng.kg-1.min-1 infusion (P less than 0.05) and remained elevated during the higher dose of ANF. Renal function was unaltered by the 10-ng.kg-1.min-1 infusion of ANF when compared with base line and placebo responses. The 25-ng.kg-1. min-1 infusion of ANF increased sodium excretion 100% from base line (P less than 0.05), whereas potassium excretion decreased 47% (P less than 0.05). Urine output increased significantly from 7.7 +/- 0.6 to 12.5 +/- 0.7 ml/min (P less than 0.05). These responses were not observed in the placebo group or in an additional group of four volunteers who received a continuous low-dose infusion of ANF (10 ng.kg-1.min-1) for two consecutive 45-min periods. Neither dose of ANF altered creatinine clearance or free water clearance. The data indicate that fivefold elevations (physiological levels) of plasma ANF do not influence renal or hormonal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic, renal, and hormonal responses to incremental ANF infusions in humans. 252 66


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