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)

Plasma levels of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP), and the plasma renin activity (PRA) were examined in 15 vascularly decompensated patients suffering from liver cirrhosis, before and after administration of albumin and after a subsequent administration of furosemide. The initial ANP level was lower in 9 patients (group "A") and higher in 6 patients (group "B") than in healthy controls (Group "A": 19.5 +/- 3.0 fmol/ml; group "B": 36.7 +/- 3.9 fmol/ml; control: 25.8 +/- 2.4 fmol/ml). The initial PRA (4.4 +/- 1.0 ng AngI/ml/h) and AVP (8.5 +/- 1.5 pg/ml) activity in group "A" increased significantly compared to group "B" (PRA: 0.44 +/- 0.09; AVP: 4.1 +/- 0.5), indicating an intravascular volume depletion in group "A". Albumin infusion raised the urine and sodium excretion and the plasma concentration of ANP in group "A" but lowered in plasma levels of renin and vasopressin. The same parameters were not changed by albumin in group "B". Furosemide equally raised the urine flow rate and sodium excretion in both groups. Plasma ANP level depends on the intravascular volume, and the secondary change in its plasma concentration plays a considerable role in the retention of fluid and electrolytes in patients with cirrhosis. The increased intravascular volume in these patients depletes the fluid and electrolyte retention via the increase in ANP level.
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PMID:Alterations of vasoconstrictor and sodium-regulating hormone systems in vascularly decompensated liver cirrhosis. 297 Jun 21

Alpha 2-adrenoceptor agonists attenuate vasopressin-mediated changes in water excretion. The effects on sodium excretion, however, are unclear. We therefore utilized the nonrecirculating isolated perfused rat kidney to study the direct effects of vasopressin and alpha 2-adrenoceptor stimulation on sodium and water excretion in the absence of systemic regulatory systems. The perfusate was a Krebs-Henseleit solution (3.5 g/100 ml Ficoll; 1.0% albumin; 36 degrees C) containing prazosin (30 nM) and propranolol (100 nM) to prevent effects of alpha 1- and beta-adrenoceptor stimulation. Vasopressin (10 microU/ml) produced a significant (P less than 0.05) decrease in both water and sodium excretion. Potassium excretion was not significantly altered. Alpha 2-Adrenoceptor stimulation with l-epinephrine (28 nM) reversed (P less than 0.05) the effects of vasopressin on water and sodium excretion. To confirm that this attenuation was mediated by alpha 2-adrenoceptors, an alpha 2-adrenoceptor antagonist, yohimbine, was administered. Yohimbine (300 nM) blocked the effects of epinephrine on sodium and water excretion (P less than 0.05). The adenosine P-site agonist, SQ 22,536 (100 microM), which mediates its effects through inhibition of adenylate cyclase, produced the same reversal as that of epinephrine on vasopressin-mediated changes. Thus alpha 2-adrenoceptor stimulation antagonized the effects of vasopressin on both water and sodium excretion at the renal level. A corollary to this conclusion is that the function-specific activation of renal adenylate cyclase determines the effect of alpha 2-adrenoceptor stimulation.
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PMID:Alpha 2-adrenoceptor antagonism of vasopressin-induced changes in sodium excretion. 298 46

Renal alpha 2-adrenoceptor stimulation by epinephrine infusion reverses cyclic adenosine monophosphate-mediated effects of vasopressin on sodium and water excretion. We used this response to determine whether renal nerve stimulation can activate renal alpha 2-adrenoceptors in the non-recirculating isolated perfused rat kidney (Krebs-Henseleit solution; 3.5 g/100 ml Ficoll; 1 g/100 ml albumin; 36 degrees C; propranolol 100 nM). In the presence of alpha 1-adrenoceptor blockade with prazosin (30 nM) alpha 2-adrenoceptor stimulation with epinephrine reversed the cyclic adenosine monophosphate-mediated effects of vasopressin on sodium (P less than 0.05) and water (P less than 0.05) excretion. Subthreshold (for vasoconstriction) renal nerve stimulation (10 V; 1 msec; 0.65 +/- 0.10 Hz) failed to alter the effect of vasopressin. Similarly, higher levels of renal nerve stimulation [plus prazosin (100 nM) or phenoxybenzamine (1.0 mg/kg per hr) to block alpha 1-adrenoceptors] did not activate renal alpha 2-adrenoceptors which are associated with the antagonism of the effects of vasopressin. The same level of subthreshold renal nerve stimulation (0.85 +/- 0.14 Hz) in the absence of vasopressin, and without alpha 1- or alpha 2-adrenoceptor blockade, decreased (P less than 0.05) sodium and water excretion. The reversal of this effect by alpha 1-adrenoceptor blockade (prazosin 30 nM) but not alpha 2-adrenoceptor blockade (yohimbine 300 nM) indicates that this effect of renal nerve stimulation is mediated through alpha 1-adrenoceptors. Thus, subthreshold renal nerve stimulation in the rat kidney induces sodium and water retention through activation of alpha 1-adrenoceptors, as shown by others in the rabbit and dog.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal nerve stimulation causes alpha 1-adrenoceptor-mediated sodium retention but not alpha 2-adrenoceptor antagonism of vasopressin. 299 Jul 59

Energy expenditure, nitrogen excretion, and serum protein levels were studied from the time of hospital admission until 2 weeks after severe head injury in eight adolescents and four children with peak 24-hour Glasgow Coma Scale scores ranging from 3 to 8. The mean measured energy expenditure (MEE) was 1.3 times Harris and Benedict's predicted value for energy expenditure. Seventy percent of the patients achieved caloric balance (MEE X 1.2) by 4 to 14 days after injury, but balance was not consistently maintained. Five of the 12 patients had intermittent diarrhea, and two had increased gastric residuals. In five patients fluid restrictions were imposed due to either the syndrome of inappropriate secretion of antidiuretic hormone, pulmonary complications, or intracranial pressure complications. For the adolescents (aged 11 to 17 years) the mean calorie intake during the 1st week was 752 kcal/day and for the children (aged 2 to 5 years) it was 340 kcal/day. During the 2nd week the mean calorie intake for the adolescents was 1671 kcal/day and for the children was 691 kcal/day. Mean urinary nitrogen excretion was 307 mg/kg/day for the adolescents and 160 mg/kg/day for the children. The calculated mean nitrogen balance for the eight adolescents and the four younger children was -13.6 and -4.1, respectively. Mean albumin levels decreased from 2.9 gm/dl during the 1st week to 2.4 gm/dl during the 2nd week (normal 3.5 to 5.0 gm/dl). Mean total protein level during the 1st week was 5.4 gm/dl and increased to a mean of 6.0 gm/dl during the 2nd week (normal 6.0 to 7.8 gm/dl). Weight loss ranged from 2 to 26 lb during the 2-week period. From these studies it can be concluded that head injury in the child and adolescent induces a metabolic response that includes increased energy expenditure and decreased serum albumin levels similar to those observed for head-injured adults. Mean nitrogen excretion values are less than those in adults with a severe head injury.
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PMID:Nutritional support and measured energy expenditure of the child and adolescent with head injury. 311 94

To investigate whether paracentesis could be an alternative therapy for ascites, 117 cirrhotics with tense ascites were randomly allocated into two groups. Fifty-eight patients (group 1) were treated with paracentesis (4-6 L/day until disappearance of ascites) and intravenous albumin infusion (40 g after each tap). Fifty-nine patients (group 2) were treated with spironolactone (200-400 mg/day) plus furosemide (40-240 mg/day). Patients from group 2 not responding to diuretics were treated with a LeVeen shunt. After disappearance of ascites, patients from both groups were discharged from hospital and were instructed to take diuretics. Patients developing tense ascites during follow-up were readmitted to hospital and treated according to their initial schedule. Paracentesis was effective in eliminating the ascites in 56 patients from group 1 (96.5%) and did not induce significant changes in renal and hepatic function, plasma volume, cardiac index, peripheral resistance, plasma renin activity, plasma norepinephrine and antidiuretic hormone concentration, and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha. Diuretics were effective in eliminating the ascites in 43 patients from group 2 (72.8%) (p less than 0.05). Ten patients in group 1 and 36 in group 2 developed complications during their first hospital stay (p less than 0.001). This difference was due to the significantly higher incidence of hepatic encephalopathy, renal impairment, and electrolyte disturbances occurring in patients treated with diuretics. The duration of hospital stay was 11.7 +/- 1.5 days for patients from group 1 and 31 +/- 2.8 days for patients from group 2 (p less than 0.001). The two groups did not differ significantly with respect to the probability of requiring readmission to hospital during follow-up, reasons for readmission, survival probability after entry into the study, and causes of death. These results indicate that paracentesis associated with intravenous albumin infusion is a fast, effective, and safe therapy for ascites in patients with cirrhosis.
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PMID:Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study. 329 7

The roles of the antidiuretic hormone arginine-vasopressin (AVP), atrial natriuretic peptide (ANP), renin, aldosterone and catecholamines in the pathogenesis of impaired water excretion were studied in edematous children with nephrotic syndrome. Compared to non-proteinuric children with nephrotic syndrome in remission, edematous children during relapse had lower serum concentrations of sodium and chloride with lower plasma osmolality, but had higher hematocrit values (P less than 0.05, each). Plasma concentration of AVP was higher in edematous children (P less than 0.01). Compared to healthy, normal children, edematous nephrotic children had higher plasma concentrations of AVP, aldosterone, renin, noradrenaline, and adrenaline (P less than 0.01, each), but had similar levels of plasma ANP. Head out water immersion and infusion of 5 ml/kg 20% human serum albumin solution, both procedures known to increase central blood volume, resulted in a reduction of elevated hormone concentrations to near-normal levels and caused a rise in sodium and water excretion. Following albumin infusion, mean ANP rose fivefold, and plasma concentrations of this hormone correlated positively with urine flow (r = 0.64, N = 18, P less than 0.01) and with sodium excretion (r = 0.62, N = 18, P less than 0.01). It is concluded that AVP, renin, aldosterone and catecholamines are stimulated in edematous children with nephrotic syndrome by reduction in effective circulatory blood volume. Central blood volume expansion induced either by water immersion or by infusion of concentrated albumin solution is able to correct elevated hormone levels and to induce salt and water excretion. Plasma ANP appears to trigger the diuretic and natriuretic effects of central volume expansion.
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PMID:Hormonal regulation of water metabolism in children with nephrotic syndrome. 330 10

Classical techniques for studying modulations of microvascular permeability have a time resolution of minutes. A newly developed method allows continuous measurement of the electrical resistance of the microvascular membrane in vivo (Olesen & Crone 1983). The technique exploits microelectrodes impaled into the vascular lumen and is based on cable analysis of the vessel. It was applied to venules on the surface of the frog brain to test the effect on microvascular permeability of a wide variety of substances. The following agents increased ionic permeability reversibly within seconds: 5-hydroxytryptamine, bradykinin, ATP, ADP, AMP, phospholipase A2, arachidonic acid, leukotriene C4, oxygen-derived free radicals, ionophore A23187, and unbound Evans blue dye. An irreversible permeability increase was induced by protamine sulphate, neuraminidase, trypsin, melittin, and snake venoms from Crotalus durissus terrificus and Bothrops atrox. The following substances were without effect within an administration period of 5 min: histamine, epinephrine, putrescine, angiotensin II, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, vasopressin, adenosine, PGE2, PGF2 alpha, prostacyclin (PGI2), leukotriene B4, albumin, heparin, plant cytokinins, hyaluronidase, thrombin, wasp venom. Variations in pH between 5.1 and 8.6 did not change permeability. Three conclusions are drawn from the observations: (1) the permeability of cerebral microvessels can be modulated by specific agents, (2) the agents induced changes in the endothelium within a few seconds, and (3) the rapid permeability increase induced by inflammatory mediators was less than two-fold and reversible within minutes.
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PMID:Substances that rapidly augment ionic conductance of endothelium in cerebral venules. 348 16

Diabetic ketoacidosis is often associated with a temporary increase in protein excretion, but the mechanisms are not completely known. The aim of the present study was to examine the effect of acute experimental moderate ketosis on kidney function and specifically on protein handling using an infusion of 3-hydroxybutyrate in healthy subjects. Seven young healthy males were infused with sodium 3-hydroxybutyrate, the peak blood level attained being 1.96 +/- 0.53 mmol/l (SD). The pH in blood and urine rose significantly from 7.40 +/- 0.03 to 7.45 +/- 0.05 (2p less than 0.01) and from 7.29 +/- 0.79 to 8.51 +/- 0.82 (2p less than 0.01), respectively. Urinary beta-2-microglobulin excretion rose significantly from 0.038 microgram/min x/ divided by 1.9 to 0.082 microgram/min x/ divided by 1.4 (geometric mean x/ divided by tolerance factor) (2p less than 0.01) but urinary albumin excretion was unchanged. No changes were seen in blood pressure, glomerular filtration rate and renal plasma flow. A marked reduction in urine flow from 15 to 5 ml/min was noted, but could not be attributed to changes in plasma arginine-vasopressin, which was reduced before and during infusion due to considerable oral water loading. It is concluded that moderate elevation in blood ketone body levels does not induce albuminuria. It is suggested that the temporary proteinuria present in diabetic ketoacidosis may be related to acidosis per se.
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PMID:Effect of 3-hydroxybutyrate infusion on urinary protein excretion in healthy man. 352 Jul 91

Six patients with severe hyponatraemia had neurological features of hyponatraemia and pronounced hypoalbuminaemia. All had biochemical features typical of the syndrome of inappropriate secretion of antidiuretic hormone with low serum osmolality and an inappropriately high urinary osmolality. All were given infusions of whole plasma or albumin solution, or both, to restore their plasma albumin concentrations to normal, which led to a dramatic increase in plasma sodium concentrations and serum osmolality, with a concomitant fall in urinary osmolality in all patients. Neurological features were reversed in four patients. It is suggested that severe hypoalbuminaemia is an important cause of appreciable hyponatraemia; infusions of plasma and albumin in such patients may reverse the biochemical and clinical features and should form the basis of management.
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PMID:Hypoalbuminaemic hyponatraemia: a new syndrome? 393 18

1 Amiloride inhibits Na transport and short-circuit current (SCC) across the toad bladder. It is 1000 times more active at the mucosal than serosal surface. The lowest effective concentration was 10(-7)M.2. The inhibition was non-competitive with the sodium on the mucosal side of the bladder.3. Vasopressin, cyclic adenosine monophosphate (AMP) and aldosterone increased Na transport and SCC across the bladder and these effects were inhibited by amiloride.4. The antagonism of amiloride for vasopressin was non-competitive.5. Amphotericin B also increases Na transport across the bladder but its action was not changed by amiloride.6. Amiloride was without effects on SCC and diffusion potentials in bladders metabolically inhibited with CN(-) and iodoacetic acid (IAA).7. Neither plasma albumin, Ca(2+) nor adenosine triphosphate (ATP) altered the effects of amiloride.8. The only structural analogue of amiloride found to reduce SCC similarly was guanidine which was 1000 times less active. Pyrazine and a substituted pyrazine analogue were without effect. Neither guanidine nor the substituted pyrazine compound were competitive with amiloride.9. Amiloride had no effect on the osmotic permeability of the toad bladder either in the presence or absence of vasopressin.10. Na transport across the toad colon was also reduced by 10(-5)M amiloride at the mucosal surface.11. The possible mechanism of action of amiloride is discussed.
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PMID:Amiloride: a potent inhibitor of sodium transport across the toad bladder. 564 23


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