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 effects of the pig calcitonin on the kidney excretory function in normotensive (NR) and spontaneously hypertensive rats (SHR) were examined. Calcitonin injection in the dose of 0.6 U/100 g of the body mass in NR and SHR in the conditions of 6-hour spontaneous diuresis caused the increase in the urination volume due to the inhibition of the tubular water reabsorption and growth of the glomerular filtration rate. The important role in the mechanism of the decrease in the water reabsorption in SHR plays the decrease in the content of vasopressin in the blood and urea in the kidney interstitium while in NR a more marked inhibition of the water reabsorption is caused by the decrease in the concentration of both urea and sodium in the kidney layers. The natriuretic effect of calcitonin was noticed only in NR.
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PMID:[The effect of calcitonin on the mechanisms of urine formation and sodium excretion in normotensive and spontaneously hypertensive rats]. 185 46

Urinary digoxin-like immunoreactive factor (DLIF), arginine-vasopressin (AVP) and other urinary parameters were investigated under normal conditions and after the i.p. injection of the following solutions: distilled water, isotonic and hypertonic NaCl, NaHCO3, KCl and urea, at a rate of 3 ml/100 g body weight. The measurement of digoxin-like immunoreactivity by two different radioimmunoassays showed that DLIF was stimulated by all volume loads regardless of the presence or absence of osmolar compounds. This dissociation between DLIF and urinary sodium excretion suggests that DLIF may not constitute the natriuretic hormone. Moreover, a dissociation between DLIF and AVP excretion also were found, which speaks against the hypothesis of a common mechanism of stimulation for both substances.
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PMID:Urinary excretion of digoxin-like immunoreactive factor and arginine-vasopressin in rats after several osmotic loads. 186 55

We have shown that urea transport across the terminal inner medullary collecting duct (terminal IMCD) is mediated by a vasopressin-stimulated, facilitated diffusion process exhibiting properties consistent with a transporter. To investigate whether hypertonic NaCl, as exists in vivo in the inner medulla, affects urea permeability, we studied isolated perfused rat terminal IMCD segments. Perfusate and bath osmolality were varied symmetrically by adding or removing NaCl or mannitol. Urea permeability rose progressively when osmolality was increased with NaCl or mannitol from 290 to 690 mOsm/kg H2O in the absence of vasopressin; there was no further increase at 890 mOsm/kg H2O. In the presence of 10(-8) M arginine vasopressin, urea permeability increased when NaCl was added to raise osmolality from 290 to 490 mOsm/kg H2O but there was no further increase at 690 mOsm/kg H2O. When 1 mM 8-bromo cyclic AMP was added to the bath, raising NaCl still increased urea permeability. These results suggest that urea transport across the rat terminal IMCD is regulated both by vasopressin and by osmolality at values present in the renal inner medulla. Osmolality seems to activate urea transport across the rat terminal IMCD by mechanisms distinct from those of vasopressin or cyclic AMP.
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PMID:An independent effect of osmolality on urea transport in rat terminal inner medullary collecting ducts. 190 26

We examined the action of high (2 x 10(-8)M) and low (6 x 10(-9)M) concentrations of atrial natriuretic factor (ANF) on water and urea transport in the rat inner medullary collecting duct (IMCD) using the in vitro microperfusion technique. We measured the hydraulic conductivity (Lp x 10(-6) cm/atm per second) and both lumen-to-bath (Pu(lb] and bath-to-lumen (Pu(bl)) 14C-urea permeabilities (Pu x 10(-5) cm/s) in the absence and in the presence of vasopressin (VP). High concentrations of ANF were able to inhibit the maximum activity of (50 microU/ml) VP-stimulated Lp but physiological concentration of ANF inhibit only submaximum activity (10 microU/ml) of VP-stimulated Lp. The hydrosomotic effect of dibutyryl-cyclic 3.5 adenosine monophosphate (cAMP) (10(-4)M) was unchanged by high concentrations of ANF (2 x 10(-8)M). Also we found that high (10(-4)M) and low (10(-6)M) concentrations of exogenous cyclic 3,5-guanosine monophosphate (GMP) while unable to change the Lp in the absence of VP, decreased the maximum activity of VP-stimulated Lp significantly. We also found that ANF inhibits partially and in a reversible manner the VP-stimulated Pu(lg) but not the VP-stimulated Pu(bl). These results demonstrated that plasma concentrations of ANF observed during volume expansion (10(-10)M) are able to inhibit submaximum activity of VP-stimulated (10 microU/ml) Lp in the rat IMCD, this effect seems to occur before cAMP formation and it appears to be mediated by cGMP. ANF (6 x 10(-9)M) also reduced the VP-stimulated urea outflux.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of atrial natriuretic factor and cyclic guanosine monophosphate on water and urea transport in the inner medullary collecting duct. 196 94

A total of 29 patients with severe hemorrhagic fever associated with the renal syndrome were studied for impact of extracorporeal hemodialysis on the activity of the renin-aldosterone system (RAS), plasma vasopressin and osmolality and the levels of the major osmotically active agents, as well as the circadian urine output and blood pressures. In patients with oliguria there was a significant activation of RAS, an increase in plasma vasopressin ad osmolality due to the increment of the urea in presence of hyponatremia. Hemodialysis led to a temporary normalization of plasma aldosterone and vasopressin levels and a decrease in blood pressure. No significant changes were documented in the activity of the plasma renin and circadian urinary output. A direct correlation was established between the plasma osmolality and the levels of vasopressin. In patients with polyuria developed in presence of hypernatremic hyperosmia plasma vasopressin elevated and aldosterone dropped.
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PMID:[The effect of hemodialysis on the vasopressin level and on the renin-aldosterone system in patients with hemorrhagic fever with renal syndrome]. 197 Sep 14

HFRS-related oliguria brings about hyperactivity of the system hypothalamus-hypophysis-adrenals and hyperfunction of the pancreas; glucose, urea and creatinine plasma levels are elevated. Prednisolone treatment leads to diminution of ACTH and cortisol levels, elevation of glucose, insulin and C-peptide concentrations in plasma compared to prednisolone-untreated patients, producing insignificant effect on plasma levels of STH, vasopressin, aldosterone, area and creatinine. Therefore, a course administration of glucocorticoids to HFRS patients is justified only in severe collapses and hypopituitary coma confirmed by the laboratory methods.
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PMID:[Effect of glucocorticoid hormones on the status of the hypothalamo-hypophyseal-adrenal system and endocrine function of the pancreas in patients with hemorrhagic fever with renal syndrome]. 197 53

The present study was designed to test the possible role of vasopressin in the renal response to dietary protein. This possibility was suggested by the similarity of effects on renal function and morphology of chronic high-protein intake and chronic stimulation of urine concentration. Adult male Brattleboro rats, genetically unable to produce vasopressin, were fed high-protein (32% casein = HP, n = 8) or low-protein (10% casein = LP, n = 9) diet for 7 wk. Renal function was evaluated by clearance techniques based on 24-h urine collections in metabolic cages. The response to a single injection of the vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) was also tested. Kidney weight and height of the different renal zones were assessed at the end of the study. HP diet increased urea excretion nearly sevenfold. Water intake increased by 57% (P less than 0.001) and urine flow rate by 71% (P less than 0.01). Urine osmolality rose from 104 to 181 mosmol/kgH2O (P less than 0.001). At variance with what occurs in rats with endogenous vasopressin (Sprague-Dawley; Bouby, N., et al. Kidney Int 34: 4-12, 1988), HP diet increased creatinine clearance per unit body weight by only 14% and did not change free water clearance, renal mass, and height of inner stripe of outer medulla. However, the rise in urine osmolality and drop in free water clearance after DDAVP were significantly greater in HP- than in LP-fed Brattleboro rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin is involved in renal effects of high-protein diet: study in homozygous Brattleboro rats. 199 84

The present in vitro microperfusion study examined whether chlorpropamide (CPM) has a direct effect on hydraulic conductivity (Lp x 10(-6) cm/atm.sec) and 14C-urea permeability (Pu x 10(-5) cm/sec) in the middle and distal inner medullary collecting duct (IMCD) obtained from acutely water-loaded Wistar rats and rats homozygous for diabetes insipidus (DI). CPM (10(-4) M) added to the bath fluid increased the Lp in the water-loaded Wistar rats from -0.05 +/- 0.13 to 6.25 +/- 0.74 (p less than 0.01) and in the DI rats from 0.05 +/- 0.01 to 5.95 +/- 0.84 (p less than 0.01), but had no effect when it was added to the perfusate. CPM stimulated Lp in a dose-dependent manner with the threshold effect at 10(-6) M. However, the addition of CPM (10(-4) M) to submaximal concentration of VP in the bath fluid did not increase the Lp. Furthermore, CPM was unable to block the inhibitory action of PGE2 on the vasopressin (VP)-stimulated Lp. On the contrary, PGE2 blocked the CPM-stimulated Lp. CPM (10(-4) M) in the peritubular fluid was able to cause a significant rise of the Pu from 13.5 +/- 0.8 to 17.3 +/- 1.0 reversibly, which represented 16% of maximum stimulated effect produced by 50 microU/ml of VP. Thus, pharmacological doses of CPM added to the peritubular side have a direct effect on terminal IMCD increasing water and urea permeability in the absence of VP, but this drug does not potentiate the VP-stimulated water transport in the IMCD. Our results were unable to confirm the hypothesis that CPM potentiates the VP-antidiuresis by the inhibition of PGE2 action in the rat IMCD.
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PMID:Effect of chlorpropamide on water and urea transport in the inner medullary collecting duct. 200 36

Conditions like heart failure that augment the activity of neurohumoral mechanisms i.e. the renin-angiotensin systems, sympathetic nerve activity and vasopressin secretion are commonly associated with a decreased effective blood volume and a reduced renal perfusion. This leads to an increased dependence of renal hemodynamics on endogenous renal prostaglandin synthesis as a vasodilator and natriuretic counter-regulating system. We investigated the role of prostaglandins in renal functional control in an experimental setting of congestive heart failure by chronic inhibition of cyclooxygenase by indomethacin. In chronic moderate heart failure plasma levels of prostaglandin E2 and prostacyclin were unchanged whereas the urinary excretion of prostaglandin E2 was significantly increased, indicating an augmented synthesis within the kidney (Figures 1 to 3). After inhibition of prostaglandin synthesis we observed a profound increase of renal vascular resistance associated with a reduction of effective renal plasma flow and renal blood flow. This was mainly due to a constriction of the vas afferens of the glomerulum. This led to an impairment of renal function indicated by an increase of serum creatinine and blood urea nitrogen associated with a reduction of urinary flow and fluid retention (Figures 4 and 5). We also studied in a randomized, double-blind, placebo-controlled, parallel-group trial in 40 patients with congestive heart failure effects of acetylsalicylic acid (500 mg t.i.d.) on renal functional parameters. In patients with normal sodium intake acetylsalicylic acid reduced urinary prostaglandin E2 concentration by 37% which led to a reduction of daily urinary sodium excretion by 29% in comparison to placebo (Figure 6). These results clearly show the importance of vasodilator prostaglandins in the regulation of kidney function in heart failure where inhibition of cyclooxygenase results in profound deterioration of renal perfusion and kidney function and retention of fluid and sodium.
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PMID:[Role of prostaglandins in regulation of kidney function in heart failure]. 206 53

Dehydrated patients usually present with an elevated serum urea level, owing in part to increased renal reabsorption of urea mediated by antidiuretic hormone (ADH). This study was carried out in order to examine whether, during dehydration, the variations in the serum urea level could discriminate patients with central diabetes insipidus (CDI) from those with dehydration due to other causes. We studied retrospectively 27 episodes of dehydration in 23 patients with CDI and 14 episodes in 14 patients without CDI. The mean serum urea level was 2.9 mmol/L in the CDI group and 15.4 mmol/L in the patients without CDI (p less than 0.001) while the mean serum sodium level was 155 mmol/L in both groups. During dehydration, patients with CDI decreased their serum urea level (4.0 +/- 2.3 vs 2.9 +/- 1.5 mmol/L, p less than 0.001). In addition, a positive correlation was found in the patients with CDI between the magnitude of diuresis and the percentage decrease in the serum urea level compared with the level before dehydration (r = 0.70, p less than 0.001). A striking increase in the clearance of urea (0.8 +/- 1 vs 2.1 +/- 1 ml/s, P less than 0.01), which exceeded the creatinine clearance (1.8 +/- 0.5 ml/s), was observed during dehydration in the six patients in whom clearance studies were done. Therefore, our results suggest that serum urea values can be used to distinguish patients dehydrated because of CDI from those with hypertonic dehydration but without ADH deficiency and that during dehydration the reabsorption of urea is mainly dependent on the renal action of ADH.
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PMID:[Diagnostic value of the determination of blood urea in dehydrated patients with and without central diabetes insipidus]. 207 36


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