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 renal response to iso-oncotic blood volume expansion with bovine serum albumin was studied in anaesthetized homozygous Brattleboro (DI) rats after acute (1 day) pretreatment with 1 U arginine-vasopressin (AVP) compared to heterozygous controls. In AVP-treated DI (DI + AVP) rats, basal urine flow as well as urinary sodium, chloride, and potassium excretion, were not different from controls. Diuresis and kaliuresis induced by volume expansion were blunted in DI + AVP rats. However, natriuresis and chloruresis were exaggerated in DI + AVP rats. They increased faster, reached a higher maximum, but declined earlier, compared to controls. The blunted diuresis resulted in a positive volume balance by the end of the experiment in DI + AVP rats, whereas the controls showed restoration of normal balance. Significant retention of sodium and chloride was observed in controls, but not in DI + AVP rats, over the time of the experiment. DI + AVP rats lost significantly less potassium than controls during the experiment. As judged from the lithium clearance method, the exaggerated saluresis in DI + AVP rats was mainly due to a reduced proximal sodium reabsorption. Plasma immunoreactivity of atrial natriuretic peptide (ANP) rose during blood volume expansion and fell in the recovery period. It was not different between AVP-treated DI rats and controls at any time of the experiment. Inulin clearance was slightly, but not significantly, lower in DI + AVP rats and increased after blood volume expansion in DI + AVP rats only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal response to blood volume expansion in Brattleboro rats after acute treatment with vasopressin. 183 44

The distal inner medullary collecting duct (IMCD) is critical in the urinary concentrating process, in part because it is the site of vasopressin (AVP)-regulated permeability to urea. The purpose of these experiments was to develop a cell culture model of the IMCD on permeable structure and to characterize the responsiveness to AVP. Rat IMCD cells were grown to confluence on collagen-coated Millipore filters glued onto plastic rings. To assess the time required to achieve confluence, the transepithelial resistance was measured periodically and was found to be stable after 2 weeks, at a maximal value of 595 +/- 22 omega cm2. In separate monolayers the effect of AVP on inulin and urea permeability was determined. While inulin permeability was unchanged after AVP, urea permeability increased from 6.0 +/- 0.4 to peak values of 16.0 +/- 3.8 (10 nM), 23.1 +/- 3.9 (1 microM) and 28.1 +/- 4.9 (10 microM) x 10(-6) cm s-1 (n = 24). In 10 other monolayers, after the addition of 1 mM 8-Br-cAMP, urea permeability increased from 5.1 +/- 0.3 to 8.1 +/- 1.6 x 10(-6) cm s-1 and, after 8-Br-cAMP + 3-isobutyl-1-methylxanthine, to 12.2 +/- 0.7 x 10(-6) cm s-1. We conclude that rat IMCD cells grown in culture exhibit the characteristics of a 'tight' epithelium. Inulin and urea permeability are not different in the absence of AVP, consistent with high resistance junctional complexes. Furthermore, IMCD cells retain the capacity for AVP-regulated urea permeability, a characteristic feature of this nephron segment in vivo.
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PMID:Vasopressin-enhanced urea transport by rat inner medullary collecting duct cells in culture. 224 45

Renal and hemodynamic effects of an intravenous infusion of atrial natriuretic factor (ANF) (8 micrograms/h) were studied in homozygous Brattleboro rats, which lack endogenous vasopressin. Heterozygous rats were used as controls. ANF-induced increases in sodium, chloride and volume excretion were higher, whereas changes in potassium excretion were lower in homozygous, as compared to heterozygous rats. The initial decrease in arterial blood pressure after ANF infusion was greater in the homozygous group, whereas there were no differential effects on heart rate. Inulin clearance, as well as clearance and fractional excretion of lithium were not significantly different between groups. The results indicate that Brattleboro rats show an exaggerated diuretic as well as saluretic response to ANF. They suggest that these effects are localized in the distal nephron and may be due to the known anatomical abnormalities in juxtamedullary nephrons of Brattleboro rats.
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PMID:Hyperresponsiveness to atrial natriuretic factor in adult Brattleboro rats. 252 97

Two doses of synthetic atrial natriuretic peptide (0.5 and 5.0 micrograms/min) and its vehicle were infused intravenously for 4 hours in eight salt-loaded normal volunteers, and the effect on blood pressure, heart rate, renal hemodynamics, solute excretion, and secretion of vasoactive hormones was studied. The 0.5 micrograms/min infusion did not alter blood pressure or heart rate, whereas the 5.0 micrograms/min infusion significantly reduced the mean pressure by 20/9 mm Hg after 2.5 to 3 hours and increased the heart rate slightly. Inulin clearance was not significantly changed, but the mean p-aminohippurate clearance fell by 13 and 32% with the lower and higher doses, respectively. Urinary excretion of sodium and chloride increased slightly with the lower dose. With the higher dose, a marked increase in urinary excretion of sodium, chloride, and calcium was observed, reaching a peak during the second hour of the infusion. Potassium and phosphate excretion did not change significantly. A brisk increase in urine flow rate and fractional water excretion was seen only during the first hour of the high-dose infusion. Signs and symptoms of hypotension were observed in two subjects. No change in plasma renin activity, angiotensin II, or aldosterone was observed during either infusion, but a marked increase occurred after discontinuation of the high-dose infusion. In conclusion, the 5 micrograms/min infusion induced a transient diuretic effect, delayed maximal natriuretic activity, and a late fall in blood pressure, with no change in inulin clearance but a dose-related decrease in p-aminohippurate clearance. Despite large amounts of sodium excreted and blood pressure reduction, no counterregulatory changes were observed in the renin-angiotensin-aldosterone system or plasma vasopressin levels during the infusion.
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PMID:Four-hour infusions of synthetic atrial natriuretic peptide in normal volunteers. 294 72

1. Dose-response effects of arginine vasopressin on renal haemodynamics were studied in conscious and in pentobarbitone-anaesthetized rats infused with 77 mM-NaCl at 5.2 and 2.6 ml h-1 respectively. 2. Vasopressin at 0.8 pmol h-1 (100 g body weight)-1 did not have a significant effect on arterial blood pressure in conscious or anaesthetized rats. Increasing the dose to 2.5 pmol h-1 (100 g body weight)-1 induced a pressor effect in conscious rats but not in anaesthetized rats. A pressor response was observed in the latter at a dose of 10 pmol h-1 (100 g body weight)-1. 3. Pressor doses of vasopressin of 100 pmol h-1 (100 g body weight)-1 and less did not significantly alter the clearance of p-aminohippurate (PAH) in either conscious or anaesthetized rats. A dose of 1000 pmol h-1 (100 g body weight)-1 significantly decreased PAH clearance in both conscious and anaesthetized animals. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin in both conscious and anaesthetized rats. Moderately pressor doses decreased inulin clearance in conscious animals only. The highest dose administered (1000 pmol h-1 (100 g body weight)-1) decreased inulin clearance in both conscious and anaesthetized rats. 5. Pressor doses of vasopressin had a biphasic effect on the filtration fraction in conscious rats. The filtration fraction decreased with doses of vasopressin at the lower end of the pressor range but increased with the highest dose of 1000 pmol h-1 (100 g body weight)-1. In contrast the filtration fraction did not change significantly with moderate pressor doses in anaesthetized rats but was increased by doses of 100 and 1000 pmol h-1 (100 g body weight)-1. 6. It is concluded that pressor doses of vasopressin lower than 100 pmol h-1 (100 g body weight)-1 do not decrease renal plasma flow rate in conscious or pentobarbitone-anaesthetized rats. The results suggest that the inconsistent effects of vasopressin on renal blood flow reported in the literature are due, at least in part, to the wide range of doses used.
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PMID:Dose-response effects of pressor doses of arginine vasopressin on renal haemodynamics in the rat. 325 42

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.
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PMID:Renal handling of urea in subjects with persistent azotemia and normal renal function. 332

1. Dose-response effects of lysine vasopressin on renal haemodynamics were studied in conscious rats infused with 2.5% (w/v) dextrose solution at 5.8 ml/h. 2. Lysine vasopressin was maximally antidiuretic in the absence of a significant pressor effect at a dose of 2.5 pmol h-1 100 g body weight-1. Doses of vasopressin greater than this induced a dose-dependent increase in arterial blood pressure. 3. The clearance of p-aminohippurate (PAH) was not significantly changed by vasopressin, even at pressor doses. Rats pre-treated with indomethacin to inhibit prostaglandin synthesis showed a decrease in PAH clearance during the infusion of vasopressin at a dose of 30 pmol h-1 100 g body weight-1, and this suggests that the renal vasoconstrictor actions of vasopressin are attenuated by dilator prostaglandins. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin but was decreased in a dose-dependent manner by pressor doses. A maximal effect was induced by a dose of 30 pmol h-1 100 g body weight-1 which decreased inulin clearance from 3.23 +/- 0.76 (mean +/- S.E. of mean) to 1.60 +/- 0.37 ml/min (P less than 0.02). A change in inulin clearance (from 3.42 +/- 0.46 to 2.17 +/- 0.33 ml/min, P less than 0.01) was also observed in rats pre-treated with indomethacin and infused with vasopressin at the same dose. The magnitude of the change was not significantly different from that observed in rats which were not treated with indomethacin. 5. Control rats infused with dextrose showed a slight but significant increase in sodium excretion during the course of the experiment. A similar natriuresis was observed in rats infused with non-pressor doses of vasopressin but was considerably enhanced in rats infused with pressor doses of the peptide. The antidiuresis induced by vasopressin remained maximal in rats infused with pressor doses. 6. Potassium and osmolal outputs were unchanged by non-pressor doses of vasopressin but significantly increased during administration of pressor doses. 7. It is concluded that pressor doses of lysine vasopressin do not alter total renal perfusion in conscious rats when the prostaglandin system is intact. Glomerular filtration is, however, decreased in a dose-dependent manner by these amounts but the mechanism is unclear.
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PMID:Renal haemodynamic actions of pressor doses of lysine vasopressin in the rat. 344 52

Hemodynamic and hormonal factors were monitored in nine patients with nephrotic syndrome who were evaluated relative to their capacity to excrete a 20-mL/kg water load (normal greater than 80%). In five "nonexcretor" patients (37% of water load excreted in five hours), as compared to four normal excretors (105% of water load excreted in five hours; P less than .01 v nonexcretors), neither BP (131/88 v 119/79 mm Hg), pulse (74 v 77 beats/min), cardiac index (3.7 v 3.1 L/min/m2), pulmonary wedge pressure (9.3 v 7.3 mm Hg), systemic vascular resistance (1537 v 1254 dynes-sec-cm-5), nor plasma volume (41.3 v 40.1 mL/kg) were different. Similarly, plasma renin activity (2.6 v 3.7 ng/mL/h), plasma aldosterone (12 v 10.9 ng/dL), and plasma norepinephrine (403 v 312 pg/mL) were not different between nonexcretor v excretor patients with nephrotic syndrome. Plasma vasopressin concentrations were also similar both before (3.1 +/- 0.8 v 2.4 +/- 1.2 pg/mL) and during the water load (0.9 +/- 0.3 v 1.0 +/- 0.4 pg/mL). Inulin clearances, however, were lower in the nonexcretor v the excretor nephrotic patients (37 v 78 mL/min/1.73 m2; P less than .02) and correlated with water excretion (r = .68; P less than .05). Head-out water immersion increased sodium (40 to 110 microEq/min; P less than .01) and water excretion (37% to 82%; P less than .025) in the nonexcretors; the improvement correlated with the increase in inulin clearance during immersion (r = .70; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of glomerular filtration rate in the impaired sodium and water excretion of patients with the nephrotic syndrome. 352 75

Tubular sodium handling in humans undergoing hypotonic expansion due to the administration of antidiuretic hormone was studied using the clearance of lithium as an index of distal filtrate and sodium delivery. Clearance studies were performed in the morning in eight normal subjects before and on the fourth day of intranasal I-desamino-8-D-arginine vasopressin (dDAVP) administration. Fluid intake was kept constant at 25 ml/kg body weight. After dDAVP body weight increased (2.5 +/- 0.4 kg), plasma sodium fell (from 143 +/- 1 to 128 +/- 5 mmol/liter) and a progressive natriuresis developed. Sodium balance remained negative up to the second clearance study, when the cumulative sodium loss amounted to 148 +/- 96 mmol. Plasma renin activity fell significantly, but plasma aldosterone did not. Inulin clearance rose from 110 +/- 14 to 135 +/- 23 ml/min and lithium clearance from 30.9 +/- 7.6 to 48.9 +/- 15.1 ml/min. Fractional reabsorption of uric acid, phosphate and calcium decreased. Together these changes suggest that the negative sodium balance in hypotonic expansion with dDAVP results from increased filtered sodium load, decreased fractional reabsorption in the proximal tubules, and increased distal delivery. Estimated fractional reabsorption in the distal nephron remained unaltered. The plasma concentration of lithium, of which 10.8 mmol was ingested on the eve of the clearance studies, was not lower during the dDAVP-clearance study. This indicates that the tubular adaptations mentioned are present intermittently, in particular during daytime.
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PMID:Lithium clearance during the paradoxical natriuresis of hypotonic expansion in man. 366 96

The peptides vasopressin-Gly and vasopressin-Gly-Lys-Arg occur as part of the sequence of the vasopressin-neurophysin precursor molecule and may be released from the hypothalamus and/or pituitary. [8-Lysine]-vasopressin-Gly (LVP-Gly) and [8-lysine]-vasopressin-Gly-Lys-Arg were administered i.v. to conscious, water-diuretic rats. The renal effects of the peptides were assessed by comparison with the actions of [8-lysine]-vasopressin (LVP) which was administered to separate groups of rats. LVP-Gly and LVP-Gly-Lys-Arg were weakly antidiuretic. LVP-Gly-Lys-Arg was the more potent of the two peptides, but on a molar basis it only had about 10% of the antidiuretic activity of LVP. LVP-Gly and LVP-Gly-Lys-Arg at 10 pmol/h per 100 g body weight (equivalent to the maximal antidiuretic dose of LVP) slightly decreased (P less than 0.001) urine flow without causing significant changes in urine osmolality. LVP (10 pmol/h per 100 g body weight) promoted a marked natriuresis (P less than 0.001) but LVP-Gly and LVP-Gly-Lys-Arg were not natriuretic, even at the dose which was markedly antidiuretic (100 pmol/h per 100 g body weight). Osmolal output decreased at all doses during administration of the extended peptides, but was not significantly changed in the control group or by LVP. Inulin clearance was decreased by about 30% during administration of both LVP and LVP-Gly-Lys-Arg at 100 pmol/h per 100 g body weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vasopressin-glycine and vasopressin-glycine-lysine-arginine on renal function in the rat. 395 May 30


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