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)

Prolactin-releasing (PRF) activity was found in Pitressin (a commercial extract from posterior pituitary for vasopressin). Injection of Pitressin into conscious free-moving rats implanted with a permanent atrial indwelling cannula, produced a transient increase in prolactin concentration in the circulation. In order to find out whether the PRF activity was due to vasopressin or to an unidentified component in the Pitressin, we tested synthetic lysine vasopressin and demonstrated that vasopressin (1 U/kg) elevated plasma prolactin concentration about threefold. In contrast, oxytocin (1 U/kg) did not alter the prolactin concentration. In order to find out whether the effect of vasopressin is a direct or indirect action, we tested the vasopressin effect on hypophysectomized rats which had previously been implanted with 2 adenohypophyses under the kidney capsule. Again this dose (2 U/kg) of vasopressin elevated circulating plasma prolactin. These experiments indicate that vasopressin can elevate circulating prolactin concentration in nonestrogen-primed normal male rats and that vasopressin also stimulates prolactin secretion from transplanted glands dissociated from direct hypothalamic control.
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PMID:Vasopressin has a direct effect on prolactin release in male rats. 705 60

The validity of transcutaneous oxygen partial pressure (tcPO2) was tested during pharmacological vasodilatation and vasoconstriction of the skin. Measurements of transcutaneous oxygen partial pressure (tcPO2) were done on the hairless skin of the abdomen in 18 anaesthetized rabbits, when beta-pyridyl-carbonyl (Ronicol) was used as a vasodilator and vasopressin (Pitressin) as a vasoconstrictor. Vasodilation yielded no significant influence on the tcPO2-measurement. Vasoconstriction, however, resulted in a marked decrease of the tcPO2-signal (p less than 0.001). During this phase tcPO2 did no longer reflect arterial PO2 which remained nearly constant. In this experimental model vasoconstrictive drugs may cause a marked underestimation of the arterial oxygen tension. The dependence of the tcPO2-measurement on maximal local skin perfusion should be considered in intensive care patients.
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PMID:[Validity of the transcutaneous PO2-measurement during pharmacologically induced changes of skin perfusion (author's transl)]. 707 28

1. The Na+ and K+ concentrations in plasma and cerebrospinal (c.s.f.), resting potentials in skeletal muscle fibres, cardiac beat to beat intervals and 90% repolarization times were measured in Long Evans rats (parent strain controls) and in Brattleboro rats with hypothalamic diabetes insipidus (DI). 2. Cation concentration measurements confirmed previous observations that Brattleboro DI rats are mildly hypokalaemic compared with rats of the parent Long Evans strain, and indicated that the c.s.f. [Na+] is significantly raised in the former group of animals while the [K+] in the c.s.f. samples is similar in the two groups. 3. The mean resting potential of deep skeletal muscle fibres in Brattleboro DI rats was significantly more negative than the corresponding value in the Long Evans rats, and this finding was in close agreement with the difference observed for the calculated K+ equilibrium potentials in the two groups of animals. 4. The beat to beat intervals and the 90% repolarization times of cardiac action potentials were also determined in Brattleboro DI and Long Evans rats, and the mean values for both variables were significantly shorter in the former group of animals. 5. The administration of Pitressin by subcutaneous injection (500-100 mu./24 hr) to Brattleboro rats abolished the hypokalaemia and the hyperpolarization of skeletal muscle fibre membranes but had no significant effect on c.s.f. cation concentrations. 6. The present findings suggest that the absence of vasopressin in the Brattleboro DI rats results in a hyperpolarization of muscle cell membranes, and in changes in the cardiac action potential. These effects may be partly related to the mild hypokalaemia present in these animals.
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PMID:The effect of vasopressin on extracellular cation concentrations and muscle resting potentials in the rat. 732 Aug 92

Recent data have shown the role of urea in the urinary concentrating mechanism. We studied the effects of exogenous urea administration in hyponatremia associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In 20 patients with SIADH, we observed a positive correlation between serum sodium and blood urea levels (r = 0.65; p less than 0.01). In one patient with an oat cell carcinoma and SIADH-induced hyponatremia, we observed the same positive correlation (r = 0.80; p less than 0.01) but also a negative one between the excreted fraction of filtered sodium and urinary urea (r = -0.67; p less than 0.001). The short-term administration of low doses of urea (4 to 10 g) resulted in correcting the "salt-losing" tendency of this patient. Longer term administration of high doses of urea (30 g/day) was attempted with the same patient as well as with a healthy volunteer subject with Pitressin-induced SIADH. in both patients, urea treatment lowered urinary sodium excretion as long as hyponatremia was significant (less than 130 meq/liter). Urea treatment also induced a persistent osmotic diuresis, allowing a normal daily intake of water despite SIADH. This was clearly shown during the long-term treatment of a third patient with SIADH who was taking 30 g urea/day during 11 weeks. It is concluded that urea is a good alternative in the treatment of patients with SIADH who presented with persistent hyponatremia despite the restriction of water intake.
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PMID:Treatment of the syndrome of inappropriate secretion of antidiuretic hormone by urea. 738 14

Vasopressin (Pitressin) infusion through peripheral veins is a commonly used modality for control of bleeding esophageal varices. In this report we describe the development of infected gangrene at the site of accidental vasopressin infiltration in a patient with diabetes mellitus, cirrhosis and bleeding esophageal varices. Among the explanations for the development of gangrene are: 1. continuous intravenous administration; 2. diabetic peripheral vascular disease; 3. mechanical compression of extravasated fluid in a closed space. No antagonist has been clinically proven to reverse the vasoconstrictive effects of vasopressin.
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PMID:Infected gangrene. A serious complication of peripheral vasopressin administration. 741 38

Triglycyl-lysine vasopressin (tGLVPP) is activated in the circulation when the N-triglycyl residue of the molecule is cleaved by endothelial peptidases, releasing lysine vasopressin. We compared the effect of an intravenous bolus dose of tGLV (20 micrograms/kg) with a constant infusion (2.75 mU/kg/min) of arginine and lysine vasopressin (Pitressin) in normal mongrel dogs. Portal pressure was artifactually increased by a constricting flow probe. Baseline values were similar in both groups; at the time of near-maximal reduction in portal pressure, both drugs equally reduced portal venous pressure (38 +/- 4 vs 39 +/- 4%), superior mesenteric arterial blood flow (40 +/- 8 vs 39 +/- 9%), portal venous flow (35 +/- 4 vs 40 +/- 5%), and heart rate (9 +/- 2 vs 11 +/- 7%. Cardiac output obtained 10-30 min after tGLVP administration was similar that of VP, and each drug reduced cardiac output significantly when compared with its own baseline (18 +/- 4 vs 21 +/- 7%). Mean arterial pressure increased similarly with both drugs (11 +/- 3 vs 11 +/- 3%). The only difference observed was the hepatic arterial flow response. While tGLVP increased HAF 34 +/- 11%, the physiologic autoregulatory response to a decrease in portal venous flow and pressure; vasopressin was associated with no such compensatory response (1 +/- 6%). Whether this advantage of tGLVP and its more prolonged reduction of portal venous pressure (mean 103 min) are beneficial in the clinical setting requires additional studies.
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PMID:Comparison of vasopressin and triglycyl-lysine vasopressin on splanchnic and systemic hemodynamics in dogs. 741 92

[Arg8]Vasotocin (AVT) is considered to be the most primitive known vertebrate neurohypophyseal peptide of the vasopressin/oxytocin hormone family and may thus be ancestral to all the other vertebrate peptide hormones. The molecular evolution of the corresponding receptor family has now been studied by cloning an AVT receptor, consisting of 435 amino acid residues, from the teleost fish, the white sucker Catostomus commersoni. Frog oocytes injected with the AVT receptor-encoding cRNA respond to the application of AVT, but not to its structural and functional counterpart isotocin, by an induction of membrane chloride currents indicating the coupling of the AVT receptor to the inositol phosphate/calcium pathway. The pharmacological properties of the expressed AVT receptor show that it represents, or is closely related to, an ancestral nonapeptide receptor: oxytocin, aspargtocin, mesotocin, and vasopressin activated the receptor, but other members of the vasopressin/oxytocin family tested showed little or no potency; antagonists of the mammalian vasopressin V1 and oxytocin receptors blocked the AVT response. Comparison of AVT receptor sequences spanning transmembrane domains two to five, deduced by cloning cDNAs from the Pacific salmon Oncorhynchus kisutch, the cave-dwelling fish Astyanax fasciatus, and the anuran Xenopus laevis, with those of their mammalian counterparts emphasizes amino acid residues that are involved in hormone binding. The presence of a 5.0-kb transcript in various teleost tissues (pituitary, liver, gills, swim bladder, and lateral line) points to a physiological role for the fish AVT receptor in metabolic, osmoregulatory, and sensory processes.
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PMID:Structure, function, and phylogeny of [Arg8]vasotocin receptors from teleost fish and toad. 750 69

The effect of antidiuretic hormone (ADH) on a distal nephron cell line (A6) was studied using the whole cell patch clamp technique. Arginine vasotocin (AVT, 140mU/ml) evoked a "transient" increase in whole cell currents as did dibutyryl cyclic AMP (5 mM). These transients consisted of two components: one was the non-selective cation conductance and the other was the Cl- conductance. The transient was evoked by AVT in the lower cytosolic Cl- concentration ([Cl-]i) (< approximately 50 mM), and was suppressed by higher concentrations of [Cl-]i (125 mM) in A6 cells. It seems likely that the [Cl-]i maintained at a lower level is an important requirement for A6 cells to respond to AVT.
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PMID:Whole cell conductance regulated by cytosolic [Cl-] and ADH-activated Cl- channels in a distal nephron cell line (A6). 775 43

Adenylate cyclase sensitivity to neurohypophyseal hormones was investigated in isolated glomeruli and in nephron segments microdissected from collagenase-treated kidneys of Rana ridibunda. Vasotocin treatment increased adenylate cyclase activity in glomeruli and in collecting ducts and did not modify it in proximal convoluted tubules and in early and late distal tubules. In glomeruli, the hormonal stimulation resulted mainly in a decrease in the Km value for adenylate cyclase, which means a higher affinity for substrate (ATP) to the enzyme, whereas the response to forskolin was accounted for by increases both in affinity for substrate and in maximal adenylate cyclase velocity. The homologous neurohypophyseal hormones stimulated frog glomerular adenylate cyclase with the following rank order of affinities: hydrin 1 > or = AVT = AVP > or = hydrin 2 > OT > or = mesotocin > isotocin; structural analogs dDAVP, VDAVP, dVDAVP, and [Phe2,Orn8]VT had weak agonistic properties, [Thr4,Gly7]OT was inactive, and the antagonists OVTA, d(CH2)5Tyr(Et)2VAVP, and des-Gly9-d(CH2)5Tyr(Et)2VAVP inhibited hormone-induced enzyme activation with similar apparent inhibition constants. The vasotocin receptors triggering adenylate cyclase stimulation in frog glomeruli differ pharmacologically from V2 vasopressin receptors of mammalian kidneys and may also differ from V2-like vasotocin receptors of amphibian skin and urinary bladder.
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PMID:Vasotocin-sensitive adenylate cyclase in frog glomeruli. 778 59

The effect of antidiuretic hormone (ADH) on a distal nephron cell line (A6) was studied using the whole cell patch-clamp technique. A6 cells were cultured on a permeable support filter for 10-14 days in media containing 10% fetal bovine serum without supplemental aldosterone. In the unstimulated condition A6 cells had very small conductances of Na+,K+, and Cl-. Arginine vasotocin (AVT, 140 mU/ml, 280 nM) evoked a "transient" increase in whole cell currents as did dibutyryl-adenosine 3',5'-cyclic monophosphate (5 mM). These transients consisted of two components; one was the nonselective cation conductance, and the other was the Cl- conductance. Activation of these conductances was dependent on intracellular Cl- concentration ([Cl-]i). At low [Cl-]i (< or = 50 mM) both conductances were activated, whereas when [Cl-]i was 80 mM, only the Cl- conductance was activated. At high [Cl-]i (125 mM), both conductances were inhibited. It seems likely that the [Cl-]i maintained at a low level (< or = 50 mM) is an important requirement for A6 cells to respond to AVT.
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PMID:ADH-evoked [Cl-]i-dependent transient in whole cell current of distal nephron cell line A6. 784 Feb 49


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