UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.
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PMID:Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats. 794 38

To define changes in the magnocellular neuroendocrine system during lactation and pregnancy, we compared plasma levels of oxytocin (OT) and vasopressin (VP) after polyethylene glycol (PEG)-induced hypovolemia and cholecystokinin (CCK) stimulation. Conscious virgin, pregnant (day 20), and lactating (day 6) Sprague-Dawley rats were injected with either PEG (70-600 mg/ml; 35 or 70 ml/kg sc), CCK (100 micrograms/ml; 4 ml/kg ip), or vehicle and decapitated 4 h (PEG) or 5 min (CCK) later. Changes in thresholds for release of hormone and the responsiveness (slopes relating [hormone] to blood volume depletion or to plasma osmolality) of the OT and VP systems were determined using an iterative nonlinear threshold regression model. After PEG, plasma osmolality increased coincident with a decrease in blood volume, with both stimuli contributing to the rise in plasma VP and OT. Compared with virgin rats, neither the threshold nor the responsiveness of the VP system was altered by the combined stimulus, whereas the oxytocinergic system of pregnant rats was more responsive to osmotic component. Lactating rats, however, had a higher threshold for VP release and an apparent elevation of the OT threshold beyond 25% volume depletion. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT. Intraperitoneal CCK elevated plasma [OT] in each reproductive state, although the response in lactating animals was attenuated. In virgin and lactating rats, plasma levels of VP also increased slightly but significantly in response to CCK. During gestation when cardiovascular volume is expanded, both the VP and OT neuroendocrine systems were reset, enabling secretion of both hormones in response to hypovolemia with hypertonicity. During lactation, both neuroendocrine systems are reset such that greater changes in fluid balance are needed to stimulate hormone release. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT, indicative of preferential release of VP with less than a 5% (virgin, pregnant) or a 20% (lactating) loss in blood volume.
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PMID:Response of the magnocellular system in rats to hypovolemia and cholecystokinin during pregnancy and lactation. 818 79

Although endogenous opioids are thought to be involved in the regulation of vasopressin secretion, their precise role is unclear. We studied the effect of the potent nonselective opioid antagonist diprenorphine on the vasopressin response to osmotic (hypertonic saline, ip), hypovolemic (polyethylene glycol, ip), and hypotensive (sodium nitroprusside, sc) stimuli in male rats. We found that diprenorphine sc produced a time- and dose-dependent inhibition of the plasma vasopressin response to the hypovolemic stimulus. This inhibition was greatest 30 min after injection of the drug, but lasted for at least 4 h, was evident at doses as low as 0.0022 mumol/kg, and reached a maximum of about 85% of the stimulated control at a dose of 2.2 mumol/kg. Diprenorphine also inhibited the vasopressin response to an osmotic or a hypotensive stimulus, but the effect was less complete (approximately 50%), required 100-fold higher doses of the drug, and appeared to be bimodal. The potent kappa 1-selective opioid agonist U-50,488H also suppressed the vasopressin response to these stimuli, but the effect was not selective for hypovolemia, and the doses required (0.135-13.5 mumol/kg) were about 10- to 100-fold higher than those of diprenorphine. We postulate, therefore, that diprenorphine potently and preferentially inhibits the vasopressin response to an acute hypovolemic stimulus by antagonizing the effect of some endogenous opioidergic system critical in the volume control system.
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PMID:The effect of the nonselective opioid antagonist diprenorphine on vasopressin secretion in the rat. 827 62

We have shown previously that the nonselective opioid antagonist diprenorphine inhibits the vasopressin response to an acute hypovolemic stimulus in rats. To elucidate the type of endogenous opioid receptor at which this inhibition occurs, we investigated whether more selective antagonists, administered alone or in combination with diprenorphine, also inhibited the vasopressin response to hypovolemia induced by ip injection of polyethylene glycol. We found that the rise in plasma vasopressin was inhibited by the kappa-antagonist Mr 2266 BS at doses 30- to 300-fold higher than those of diprenorphine. Over the same dose range (0.003-100 mumol/kg), the kappa 1-selective antagonist norbinaltorphimine and the mu-selective antagonist naloxone had no effect or enhanced the vasopressin response, whereas the delta-antagonist ICI 154,129 had no effect. By augmenting the vasopressin response to hypovolemia, higher doses of naloxone or nor-binaltorphimine offset the inhibitory effect of concurrently administered diprenorphine. Mr 2266 BS did not facilitate, inhibit, or offset the action of diprenorphine. The results support the hypothesis that the inhibition of vasopressin by diprenorphine is due to antagonism of an opioid receptor and suggest that it is one of the recently discovered kappa-subtypes. They also suggest that the vasopressin response to acute hypovolemia is normally restrained by simultaneous activation of a distinct inhibitory pathway that is blocked by kappa 1- or mu-antagonists.
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PMID:The effect of selective opioid antagonists on vasopressin secretion in the rat. 827 69

In isolated hamster hepatocytes, ursodeoxycholic acid (UDCA) mobilized intracellular free calcium ([Ca2+]i) and activated phosphorylase a with a half-maximally effective concentration of 188 and 9 microM, respectively. Addition of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) did not affect the maximum [Ca2+]i mobilized by UDCA; however, [Ca2+]i returned to basal levels in 4-5 min compared with > 10 min in the absence of EGTA. Both UDCA and vasopressin activated phosphorylase a to the same extent in the presence and absence of extracellular Ca2+, and the effect of both agents was abolished when the cells were depleted in Ca2+. Vasopressin (100 nM) did not further mobilize [Ca2+]i or activate phosphorylase a when combined with 500 microM UDCA. However, unlike vasopressin, UDCA did not stimulate inositol 1,4,5-trisphosphate (IP3) formation. In contrast to taurine-conjugated UDCA (TUDCA), concentration < or = 500 microM of glycine-conjugated UDCA (GUDCA) did not affect either [Ca2+]i or phosphorylase a. Lithocholic acid and taurolithocholic acid (TLCA) displayed the highest affinity for Ca2+. In addition, TLCA, chenodeoxycholic acid, and NaF stimulated Ca2+ efflux at concentrations as low as 100 microM, 200 microM, and 5 mM, respectively. Conversely, UDCA, TUDCA, and GUDCA presented the lowest affinity for Ca2+ and had no effect on Ca2+ efflux. The 28% increase in Ca2+ release induced by TLCA alone was further augmented to approximately 60% when TLCA was combined with UDCA, TUDCA, or GUDCA. However, Ca2+ efflux induced by NaF was not further increased by UDCA and its conjugates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ursodeoxycholate mobilizes intracellular Ca2+ and activates phosphorylase a in isolated hepatocytes. 844 7

Cadmium, a trace element from natural and industrial sources, may contribute to the pathogenesis of arterial hypertension. We evaluated the effect induced by acute intracerebroventricular (icv) administration of cadmium on mean blood pressure of normotensive conscious rats. Intracerebroventricular cadmium (1 to 10 micrograms) produced a dose-dependent, sustained increase in mean blood pressure. The hypertensive response to icv cadmium was significantly (P < .01) prevented by icv pretreatment with verapamil (10 to 100 micrograms). A preventive effect was exerted also by icv nifedipine (100 micrograms); however, this result was attributable, at least in part, to the antihypertensive action of the vehicle, polyethylene glycol. The hypertensive response to icv cadmium was blunted by icv administration of 10 ng clonidine, 10 micrograms vasopressin antagonist, or 10 micrograms bradykinin antagonist (P < .05), but it was not altered by icv enalaprilat (100 micrograms). These results indicate that brain calcium channels play a role in the hypertensive action induced by icv cadmium. Accumulation of cadmium in the brain caused by prolonged exposure to this heavy metal might lead to chronic arterial hypertension.
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PMID:Verapamil prevents the acute hypertensive response to intracerebroventricular cadmium in conscious normotensive rats. 846 5

This study demonstrates how the common pharmaceutical wetting agent sodium dodecyl sulfate (SDS) increases the absorption of drugs and peptides across the human intestinal epithelium. First, an assay that could follow the reversible and irreversible time-dependent effects of SDS on the permeability of Caco-2 cell monolayers with high reproducibility was developed. SDS (0.40 mM) exposure for 20 min resulted in reversible absorption enhancement of mannitol (M(r), 182 g/mol), 1-deamino-8-D-arginine-vasopressin (M(r), 1071 g/mol), and polyethylene glycol (M(r), 4000 g/mol). A longer (2 h) exposure to SDS resulted in irreversible absorption enhancement. Second, transepithelial electrical resistance measurements (TEER) together with fluorescence and transmission electron microscopy were used to study the effects of SDS on epithelial integrity, cell membranes, intracellular calcium concentration, cytoskeleton, and tight junctions. The effect of SDS (0.40 mM) on epithelial integrity was immediate. A significant decrease in transepithelial electrical resistance measurements was obtained with 1 min after exposure to SDS that was concomitant with increases in the permeability of the apical cell membranes and intracellular calcium concentration. SDS shortened the microvilli of the cells and produced apical (but not basolateral) membrane wounds, actin disbandment, disorganization of the terminal web, and structural separation of the tight junctions. The absorption enhancement was not reduced after repair of the apical cell membranes, indicating that SDS enhances drug and peptide absorption across the intestinal epithelium by the paracellular pathway.
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PMID:Epithelial transport of drugs in cell culture. VIII: Effects of sodium dodecyl sulfate on cell membrane and tight junction permeability in human intestinal epithelial (Caco-2) cells. 846 83

1. Male, vasopressin-deficient, normotensive (DI/N) and hypertensive (DI/H) rats were chronically instrumented (all surgery under sodium methohexitone anaesthesia) to allow assessment of resting haemodynamic status and responses to antagonism of AT1-receptors (Experiment 1), ET(A-) and ET(B-) receptors (Experiment 2) or adrenoceptors (Experiment 3). 2. Before any treatment, mean arterial blood pressure (MAP) was higher, and hindquarters vascular conductance was consistently lower in all groups of DI/H rats than in DI/N rats. 3. In Experiment 1, losartan (10 mg kg-1 i.v.), an AT1-receptor antagonist, was given 5 h after s.c. injection of saline, (DI/N, n = 8; DI/H, n = 8) or hyperoncotic polyethylene glycol, (DI/N, n = 9; DI/H, n = 9) to induce isosmotic hypovolaemia. In the volume-replete state, losartan caused similar small falls in MAP in the two groups (maximum delta MAP; DI/N, -9 +/- 2; DI/H, -15 +/- 5 mmHg), but the mesenteric and hindquarters vasodilatations were greater in DI/N rats. In the volume-depleted state the effects of losartan were augmented (delta MAP; DI/N, -32 +/- 3; DI/H. -31 +/- 3 mmHg), but its vasodilator effects were still greater in DI/N than in DI/H rats. 4. In Experiment 2, infusion of the ET(A-)ET(B-)receptor antagonist, SB 209670 (600 micrograms kg-1 h-1; DI/N, n = 8; DI/H, n = 9), had haemodynamic effects that were not different from those during saline infusion in DI/N (n = 7) and DI/H rats (n = 8). 5. In Experiment 3, sequential administration of the beta 2-adrenoceptor antagonist, ICI 118551 (0.2 mg kg-1 bolus, 0.1 mg kg-1 h-1 infusion), the alpha 2-adrenoceptor antagonist, idazoxan (0.75 mg kg-1 bolus, 1 mg kg-1 h-1 infusion), and losartan (10 mg kg-1 bolus) had only slight haemodynamic effects in DI/N (n = 8) and DI/H (n = 9) rats. Subsequent administration of the alpha 1-adrenoceptor antagonist, prazosin (0.5 mg kg-1 bolus, 0.8 mg kg-1 h-1 infusion) caused marked hypotension, although MAP was still higher in DI/H (95 +/- 4 mmHg) than in DI/N (75 +/- 4 mmHg) rats. However, in this circumstance there were no significant differences between renal, or mesenteric, or hindquarters vascular conductances in the two groups. 6. The results indicate that the hypertension and hindquarters vasoconstriction in DI/H rats is not dependent on AII or endothelin. Moreover, the relative elevation in MAP in DI/H persists in the presence of antagonism of beta 2, alpha 2- and alpha 1-adrenoceptors, in spite of no significant difference in regional vascular conductances.
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PMID:Regional haemodynamic effects of antagonists of angiotensin II, endothelin and adrenoceptors in conscious, vasopressin-deficient, genetically hypertensive rats. 873 34

Pinealectomy has been shown to alter daily rhythms of neurohypophysial hormone release, with plasma hormone concentrations being elevated in the morning, as compared to intact rats. To determine whether pineal removal also altered the response to known stimuli of hormone release, vasopressin concentrations were measured in control, sham-operated, and pinealectomized animals during extracellular fluid hypertonicity produced by an intraperitoneal (i.p.) injection of hypertonic saline or hypovolaemia produced by an i.p. injections of polyethylene glycol. In the combined sham-operated and unoperated groups, injection of hypertonic saline produced a marked increase in plasma vasopressin concentrations from 2.18 +/- 0.28 to 7.2 +/- 1.24 pmol/liter, but the response was attenuated in pinealectomized animals, concentrations increasing to only 3.4 +/- 1.2 pmol/liter. Similarly, following infusion of hypertonic saline, the increase in plasma vasopressin per unit increase in plasma sodium was lower in pinealectomized animals than the pineal intact controls. The response to hypovolaemia was also attenuated, plasma hormone concentrations following reduction in blood volume of approximately 10% increasing to only 3.6 +/- 0.6 pmol/liter as compared to 7.3 +/- 2.2 pmol/liter in the control groups. There were no significant differences in pituitary vasopressin content in any of the groups studied. Thus, the pineal may influence the vasopressin response to physiological stimuli.
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PMID:Release of vasopressin in response to altered plasma volume and sodium concentrations following pinealectomy in the rat. 883 55

Ionic mechanisms responsible for histamine-induced prolonged depolarization in supraoptic nucleus neurons were investigated using whole-cell patch recordings in horizontally prepared brain slices from adult male rats. Bath application of histamine (1-10 microM) in control medium induced membrane depolarization in nine of 12 phasically firing, putative vasopressin cells, but not in continuous firing, putative oxytocin cells (none of five cells). Depolarization, usually accompanied by increased firing rate, started within 20 s after histamine reached the slices, lasting for 3-13 min, after which they repolarized, and this was repeatable upon washout. Chelation of intracellular Ca2+ with 11 mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetate and perfusion of slices with Ca(2+)-free medium blocked neither histamine-induced membrane depolarizations nor increased firing rates in 24 of 30 cells recorded. Depolarizations were always associated with decreases in membrane conductance. Following treatment with promethazine (H1 receptor antagonist) in six cells excited previously by histamine, subsequent application induced neither membrane depolarization nor increased firing. H1 receptor agonists mimicked histamine-induced depolarization (four of six cells) but the H2 receptor agonist, dimaprit (10 microM), had no effect (all of nine cells). In medium containing 0 mM Ca2+, 2 mM Co2+ and 1-2 microM tetrodotoxin, with internal Ca2+ chelation, bath application of histamine induced an apparent inward current in 15 of 20 supraoptic neurons tested. The peak of inward current evoked by 1-10 microM histamine at holding potentials around -50 mV varied from 10 to 50 pA (27.3 +/- 0.3 pA, mean +/- S.E.M.). Ramp voltage tests revealed that this inward current decreased as membrane potential was hyperpolarized and had a reversal potential of -90.1 +/- 3.8 mV (n = 10). Subtraction of current obtained before from that during histamine application revealed a current that was linear against membrane potential. Increasing external K+ concentration or introduction of K+ channel blockers in the medium attenuated or abolished histamine-induced inward current at membrane potentials close to -50 mV. When external Cl- concentration was reduced, histamine-induced inward current was still seen in five of seven supraoptic cells tested. Neither inward current nor change in conductance was observed following bath application of histamine in 11 of 12 neurons recorded using patch pipettes containing guanosine 5'-O-(2-thiodiphosphate), and in seven of eight neurons using pipettes containing guanosine 5'-O-(3-thiotriphosphate). These results suggest that histamine depolarizes supraoptic neurons, at least in part, by inhibiting a K+ leakage current mediated by H1 receptors linked to GTP-binding proteins and Ca(2+)-independent pathways. This study provides initial evidence for the second messengers regulating K+ leakage current.
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PMID:Histamine-induced prolonged depolarization in rat supraoptic neurons: G-protein-mediated, Ca(2+)-independent suppression of K+ leakage conductance. 884 19

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