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)

We assessed sodium balance and extracellular volume regulation in very low birth weight infants by examining the effect of differences in sodium intake on postnatal sodium homeostasis and body water composition. Twenty infants (mean birth weight 1103 +/- 216 gm, mean gestation 28.5 +/- 1.7 weeks) were randomly assigned to receive sodium in doses of either 1 or 3 mmol.kg-1.day-1 for the first 10 postnatal days. Extracellular volume (estimated by the bromide dilution method), sodium excretion, creatinine clearance, fractional sodium excretion, plasma atrial natriuretic factor level, urine aldosterone concentration, and vasopressin excretion were measured on postnatal days 1, 5, 10, 20, and 30. The corrected bromide space was large at birth and decreased in both groups during the first 5 days of observation, concomitant with a negative sodium balance. After 5 days of age, sodium excretion decreased in both groups so that sodium balance became positive and the corrected bromide space increased in proportion to increasing body weight. Differences in sodium intake were associated with differences in tubular sodium reabsorption; corrected bromide space and net sodium balance were similar in the two groups. Serum sodium concentration was significantly lower in the low-sodium intake group. Creatinine clearance, plasma atrial natriuretic factor level, and excretion of aldosterone and vasopressin were not significantly different between the two groups. We conclude that very low birth weight infants are able to regulate sodium balance by altering renal sodium excretion. However, the renal response to sodium intake may be insufficient to prevent changes in serum sodium concentration. The roles of specific renal and hormonal mechanisms regulating sodium excretion in very low birth weight infants remain incompletely defined.
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PMID:Sodium balance and extracellular volume regulation in very low birth weight infants. 252 66

Blood flow in the superior mesenteric artery was observed with a chronically implanted electromagnetic flow probe in two-kidney, one-clip renovascular hypertensive rats (2K1C), one-kidney, one-clip renovascular hypertensive rats (1K1C), and normotensive control rats (NCR) in the conscious state. Arterial pressure was recorded with an indwelling catheter. Superior mesenteric resistance was calculated as arterial pressure divided by superior mesenteric flow. In all three groups of rats, superior mesenteric resistance remained almost unchanged when arterial pressure decreased markedly on ganglionic blockade with hexamethonium bromide. However, subsequent injection of a vasopressin antagonist (Manning compound) decreased superior mesenteric resistance significantly in 2K1C but not in 1K1C and NCR. Injection of vasopressin antagonist alone was without effect on arterial pressure and superior mesenteric flow in the three rat groups. Only 2K1C were judged to have appreciable sympathetic tone in resistance vessels of the superior mesenteric area, which was blocked by hexamethonium but compensated for by secondarily secreted vasopressin.
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PMID:Superior mesenteric sympathetic tone in conscious renovascular hypertensive rats. 260 Nov 93

Experiments were done in alpha-chloralose-anesthetized, paralyzed and artificially ventilated cats with vagus, cervical sympathetic, aortic depressor, and carotid sinus nerves cut bilaterally to investigate the effect of afferent renal nerve (ARN) stimulation on circulating levels of vasopressin (AVP). Electrical stimulation of ARN elicited a pressor response that had two components, a primary (1 degree) component locked in time with the stimulus and a secondary (2 degree) component that had a long onset latency and that outlasted the stimulation period. The 1 degree and 2 degree components of the pressor response were largest at stimulation frequencies of 30 and 40 Hz, respectively. Autonomic blockade with hexamethonium bromide and atropine methylbromide abolished the 1 degree component. Administration of the vasopressin V1-vascular receptor antagonist d(CH2)5VAVP during autonomic blockade abolished the 2 degree component. Plasma concentrations of AVP measured by radioimmunoassay increased from control levels of 5.2 +/- 0.9 to 53.6 +/- 18.6 pg/ml during a 5-min period of stimulation of ARN. Plasma AVP levels measured 20-40 min after stimulation (13.6 +/- 7.0 pg/ml) were not significantly different from control values. Plasma osmolality was not altered during the course of the experiment. These data demonstrate that sensory information originating in the kidney alters the release of vasopressin from the neurohypophysis and suggest that ARN are an important component of the neural circuitry involved in homeostatic mechanisms controlling arterial pressure.
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PMID:Effect of stimulation of afferent renal nerves on plasma levels of vasopressin. 288 95

We studied the effects of cyclic AMP (cAMP) on HCO-3 transport by rabbit cortical collecting tubules perfused in vitro. Net HCO-3 secretion was observed in tubules from NaHCO3- loaded rabbits. 8-Bromo-cAMP-stimulated net HCO-3 secretion, whereas secretion fell with time in control tubules. Both isoproterenol and vasopressin (ADH) are known to stimulate adenylate cyclase in this epithelium; however, only isoproterenol stimulated net HCO-3 secretion. The mechanism of cAMP-stimulated HCO-3 secretion was examined. If both HCO-3 and H+ secretion were to occur simultaneously in tubules exhibiting net HCO-3 secretion, cAMP might increase the net HCO-3 secretory rate by inhibiting H+ secretion, by stimulating HCO-3 secretion, or both. These possibilities were examined using basolateral addition of the disulfonic stilbene (4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS). In acidifying tubules from NH4Cl-loaded rabbits, DIDS eliminated HCO-3 reabsorption, a result consistent with known effects of DIDS as an inhibitor of H+ secretion. In contrast, cAMP left acidification (H+ secretion) intact. DIDS applied to HCO-3 secretory tubules failed to increase the HCO-3 secretory rate, indicating minimal H+ secretion in HCO-3 secreting tubules. Thus, inhibition of H+ secretion by cAMP could not account for the cAMP-induced stimulation of net HCO-3 secretion. cAMP-stimulated HCO-3 secretion was reversibly eliminated by 0 Cl perfusate, whereas luminal DIDS had no effect. Bath amiloride (1 mM) failed to eliminate cAMP-stimulated HCO-3 secretion when bath [Na+] was 145 mM or 5 mM. cAMP depolarized the transepithelial voltage. The collected fluid [HCO-3] after cAMP could be accounted for by electrical driving forces, suggesting that cAMP stimulates passive HCO-3 secretion. However, cAMP did not alter HCO-3 permeability measured under conditions expected to inhibit transcellular HCO-3 movement (0 Cl- solutions and bath DIDS). This measured HCO-3 permeability was not high enough to account, by passive diffusion, for the HCO-3 fluxes observed in Cl-containing solutions. We conclude the following: cAMP increased net HCO3- secretion by stimulating HCO3- secretion and not by inhibiting H+ secretion; this HCO3- secretion may have occurred by Cl-HCO3- exchange; Na+-H+ exchange appeared not to play a role in basolateral H+ extrusion under these conditions; and the stimulation of HCO3- secretion by isoproterenol, but not ADH, suggests the existence of separate cell cAMP pools or cellular heterogeneity in this cAMP response.
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PMID:Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules. 298 40

The short-term interactions of insulin and vasopressin on pyruvate kinase (PK) activity were studied in primary cultures of rat hepatocytes. (1) Vasopressin inhibited PK activity by approx. 30% within 15 s, but activity returned to control values by 5 min. The transient inhibition by vasopressin was mimicked by either 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) or ionophore A23187. (2) Insulin alone transiently inhibited PK activity at 1 min, but stimulated PK activity at 5 and 15 min. (3) Insulin completely antagonized the early inhibition by vasopressin, PMA or A23187 of PK activity at 15 s. (4) Insulin inhibited PK activity in the presence of vasopressin, PMA or A23187 at 5 min. (5) 8-Bromo cyclic AMP inhibited PK activity within 15 s, and this inhibition was maintained for at least 5 min. Insulin did not antagonized the inhibition by the cyclic AMP analogue. These results show that insulin under appropriate conditions can act as an inhibitor or activator of PK.
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PMID:Insulin regulation of pyruvate kinase activity in cultured rat hepatocytes, in the presence of vasopressin, ionophore A23187 or 4 beta-phorbol 12 beta-myristate 13 alpha-acetate. 313 74

Rats were given bilateral injections of colchicine into the area of the nucleus basalis. Colchicine produced dose-dependent alterations in the acquisition of a food-reinforced working-memory task. Colchicine-induced deficits in maze performance were attenuated by cholinergic agents, including physostigmine, RS-86 (2-ethyl-8-methyl-2,8-diazospiro-(4,5)-decan-1,3-dione-hydro bromide) and nicotine. Naloxone and vasopressin did not affect radial-arm maze performance of colchicine-treated rats. Subsequent neurochemical analysis showed that colchicine decreased choline acetyltransferase (ChAT) activity and levels of norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid, serotonin and 5-hydroxyindoleacetic acid in the neocortex. However, ChAT activity and other neurochemical measures were not altered in the hippocampus or corpus striatum. Histological assessment indicated damage limited to the injection in the area of the nucleus basalis and enlarged cerebrolateral ventricles. These data suggest the possible utility of the colchicine model in the study of cognitive deficits associated with neurodegenerative diseases.
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PMID:Radial-arm maze deficits produced by colchicine administered into the area of the nucleus basalis are ameliorated by cholinergic agents. 334 52

The exposure of perfused rat livers to depolarizing concentrations of K+ (60 mM) by partial substitution of the NaCl in the medium with KCl induces glycogenolysis, respiratory changes and vasoconstriction. These responses were found to be inhibited 70-80% by 20 microM indomethacin and by 20 microM bromophenacyl bromide. This suggests that eicosanoids, namely prostaglandins, are involved in mediating these effects, and hence that the action of K+ involves primarily an effect on eicosanoid-producing cells (Kupffer and endothelial cells) within the liver. A 5 min pre-exposure of perfused livers to depolarizing concentrations of K+ (in the presence of indomethacin) was found to inhibit (by approx. 85%) the influx of Ca2+ induced by the co-administration of 10 nM glucagon and 10 nM vasopressin. A similar result was observed in isolated hepatocytes. The inhibition was probably not due to a decrease in the concentration of Na+ in the medium since the substitution of 80 mM NaCl with 80 mM choline chloride resulted in significantly less inhibition (30-40%). These results suggest that under these conditions the influx of Ca2+ in liver occurs through a pathway that is inhibited by high K+ concentration and/or a depolarization of the plasma membrane.
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PMID:Exposure to depolarizing concentrations of K+ inhibits hormonally-induced calcium influx in rat liver. 339 Jan 84

Vasotocin-associated neurophysin (MSEL-neurophysin) from the frog Rana esculenta has been isolated and sequenced through tryptic and staphylococcal proteinase peptides and cyanogen bromide fragments. This protein appears homologous to the mammalian vasopressin-associated neurophysin with a C-terminal glycopeptide extension homologous to the mammalian copeptin. In contrast to the two-step processing of mammalian vasopressin/MSEL-neurophysin/copeptin precursor, a single cleavage is therefore involved in the processing of the amphibian vasotocin/neurophysin precursor. It appears that the physiological release of the vasopressin-like hormone from the N-terminal end of the protein precursor is not dependent upon a previous trimming of the C-terminal copeptin-like moiety.
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PMID:One-step processing of the amphibian vasotocin precursor: structure of a frog (Rana esculenta) "big" neurophysin. 350 Dec 88

12-O-Tetradecanoyl-phorbol-13-acetate (TPA) stimulates glycogenolysis in perfused rat liver. The effect of TPA was blocked by indomethacin and bromophenacyl bromide. The effect of TPA on glucose output was transient in spite of the continuous presence of the phorbol ester in the perfusion medium. Addition of platelet activating factor (PAF) after the effect of TPA did not stimulate glycogenolysis. In contrast, vasopressin was able to stimulate glucose output under these conditions. Interestingly, as previously reported, PAF produced also transient stimulation of glycogenolysis; the addition of TPA after the effect of PAF had declined, was also unable to increase glucose output by the liver. It is suggested that both PAF and TPA stimulate hepatic metabolism through the generation of cyclooxygenase products.
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PMID:Stimulation of hepatic glycogenolysis by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) via cyclooxygenase products. 393 97

Platelet-activating factor (PAF) stimulates glycogenolysis and induces vasoconstriction in perfused rat liver. The effect of PAF was rapid but transient and it was blocked by indomethacin and bromophenacyl bromide which suggests a role of cyclooxygenase metabolites in its action. The homologous desensitization of glycogenolysis produced by PAF and the sensitivity of its actions to inhibitors of cyclooxygenase and phospholipase A2 markedly differentiate the mechanism of action of this agent with that of alpha 1-adrenergic agents, vasopressin or angiotensin II. No effect of PAF in isolated hepatocytes was observed which suggest that cells other than hepatocytes could be involved in its action in perfused liver. In addition nordihydroguaiaretic acid and bromophenacyl bromide abolished the vascular effect (but not the glycogenolysis) produced by epinephrine which suggest a role for lipoxygenase products in this effect.
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PMID:Possible involvement of cyclooxygenase products in the actions of platelet-activating factor and of lipoxygenase products in the vascular effects of epinephrine in perfused rat liver. 643 14


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