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)

Whereas adenosine itself exerted independent stimulatory and inhibitory effects on the adenylate cyclase activity of a platelet particulate fraction at low and high concentrations respectively, 2-substituted and N6-monosubstituted adenosines had stimulatory but greatly decreased inhibitory effects. Deoxyadenosines, on the other hand, had enhanced inhibitory but no stimulatory effects. The most potent inhibitors found were, in order of increasing activity, 9-(tetrahydro-2-furyl)adenine (SQ 22536), 2',5'-dideoxyadenosine and 2'-deoxyadenosine 3'-monophosphate. Kinetic studies on prostaglandin E1-activated adenylate cyclase showed that the inhibition caused by either 2',5'-dideoxyadenosine or compound SQ 22536 was non-competitive with MgATP and that the former compound, at least, showed negative co-operativity; 50% inhibition was observed with 4 micron-2',5'-dideoxyadenosine or 13 micron-SQ 22536. These two compounds also inhibited both the basal and prostaglandin E1-activated adenylate cyclase activities of intact platelets, when these were measured as the increases in cyclic [3H]AMP in platelets that had been labelled with [3H]adenine and were then incubated briefly with papaverine or papaverine and prostaglandin E1. Both compounds, but particularly 2',5'-dideoxyadenosine, markedly decreased the inhibition by prostaglandin E1 of platelet aggregation induced by ADP or [arginine]vasopressin as well as the associated increases in platelet cyclic AMP, so providing further evidence that the effects of prostaglandin E1 on platelet aggregation are mediated by cyclic AMP. 2'-Deoxyadenosine 3'-monophosphate did not affect the inhibition of aggregation by prostaglandin E1, suggesting that the site of action of deoxyadenosine derivatives on adenylate cyclase is intracellular. Neither 2',5'-dideoxyadenosine nor compound SQ 22536 alone induced platelet aggregation. Moreover, neither compound potentiated platelet aggregation or the platelet release reaction when suboptimal concentrations of ADP, [arginine]vasopressin, collagen or arachidonate were added to heparinized or citrated platelet-rich plasma in the absence of prostaglandin E1. These results show that cyclic AMP plays no significant role in the responses of platelets to aggregating agents in the absence of compounds that increase the platelet cyclic AMP concentration above the resting value.
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PMID:Inhibition of adenylate cyclase by adenosine analogues in preparations of broken and intact human platelets. Evidence for the unidirectional control of platelet function by cyclic AMP. 21 36

PGE1 and PGE2 are known to interfere with the water permeability effect of vasopressin in toad bladder and kidney. It has been proposed that endogenous prostaglandin E (PGE), synthesized within cells of vasopressin-sensitive tissues, serves to modulate the permeability changes elicited by the neurohypophyseal hormone. Direct evidence in support of this hypothesis is as follows: vasopressin increases the biosynthesis of PGE2 in renal interstitial cells and in isolated toad bladder. In the latter, inhibition of vasopressin-induced synthesis of PGE by a variety of inhibitors results in a greater water permeability response to vasopressin. It appears that vasopressin has two effects in toad bladder and kidney: (i) it activates adenylate cyclase thereby increasing the concentration of adenosine 3',5' monophosphate (cyclic AMP), the nucleotide responsible for the resultant increase in water permeability; and (ii) it activates a phospholipase that serves to release arachidonic acid, the precursor of PGE2 from intracellular pools. The PGE derived from the arachidonic acid diminishes adenylate-cyclase activity, in consequence of which the response of the enzyme to vasopressin is modulated.
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PMID:Role of prostaglandin E (PGE) in the modulation of the action of vasopressin on water flow in the urinary bladder of the toad and mammalian kidney. 21 71

The prolactin (PRL)-releasing activity of porcine stalk median eminence (pSME) was characterized by an in vivo bioassay and concomitant radioi-munoassay of plasma PRL and thyrotropin (TSH) levels. Methanol extracts of pSME stimulated PRL release in 3-day estrogen-primed rats when administered by the intracarotid route in doses ranging from 0.1 to 2.0 pSME equivalents. Synthetic thyrotropin-releasing hormone (TRH) stimulated the release of PRL and TSH in the dose range of 10 to 300 ng. PRL release was greater in response to a maximally effective dose of pSME than the release elicited by a maximal dose of TRH, and pSME administered together with a greater than mazimally effective dose of TRH caused additional PRL but not TSH secretion. Lysine vasopressin and prostaglandin E1 and E2 stimulated PRL release only at doses several orders of magnitude greater than the dose present in pSME. Somatostatin inhibited the release of TSH but not that of PRL whether the stimulus employed was pSME or TRH. The effective inhibitory dose of somatostatin was also significantly greater than the reported hypothalamic content. When pSME was subjected to incubation with plasma, a treatment reported to inactivate TRH, TSH-releasing activity was destroyed to a greater extent than was PRL-releasing activity. When pSME was adsorbed onto charcoal, the supernatant solution was devoid of TRH, as determined by complete removal of a [3H]TRH marker, yet substantial PRL-releasing activity was retained. TSH-releasing activity eluted from the charcoal with methanol was considerably greater than that expected on the basis of the recovery of [3H]TRH, suggesting the presence in the crude extract of a TSH-release inhibitor or of a TSH-releasing factor other than TRH. Based on the above evidence, we conclude that crude pSME contains PRL-releasing substance(s) distinct from the tripeptide TRH.
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PMID:Dissociation of prolactin-releasing activity from thyrotropin-releasing hormone in porcine stalk median eminence. 81 52

The effects of infusions of PGE1 (30 ng/kg min-1) into the lateral cerebral ventricle were studied in the conscious, hydrated goat. The infusions caused release of antidiuretic hormone and increased renal sodium excretion. When PGE1 was infused together with hypertonic NaCl these effects became markedly enhanced and the infusion also induced drinking and a rise in the arterial blood pressure. Much weaker effects were obtained by the infusion of the hypertonic NaCl alone. This sodium-PGE1 interaction is discussed in relation to previously observed, central sodium-angiotensin II interaction. A more pronounced drinking effect was obtained in response to the intraventricular infusion of PGE1 + angiotensin II, than to the infusion of either substance separately. The PGE1 administered into the lateral cerebral ventricle did not induce any febrile response.
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PMID:Influence of prostaglandin E1 on cerebral mechanisms involved in the control of fluid balance. 97 Jan 60

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.
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PMID:Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs. 115 Aug 81

The murine receptor for luteinizing hormone (LHR) was cloned and expressed in L cells. This LHR (mature protein of 674 amino acids) is very similar to that of the rat (same length, 36 amino acid differences) but differs significantly more from that of man (673 amino acids, 109 differences). Expression of the murine LHR in L cells led to the appearance of binding sites for human chorionic gonadotropin (hCG) with a Kd of 150 pM and an LH- and hCG-stimulable adenylyl cyclase activity (EC50 = 50-100 pM hCG). Upon labeling pools of phosphoinositides with [3H]myo-inositol, L cells expressing the murine LHR responded to hCG with an increase in their rate of phosphoinositide hydrolysis (EC50 = 2,400 pM hCG). This was accompanied by an increase in intracellular Ca2+ [( Ca2+]i), as determined by the Fura2 method. This increase in [Ca2+]i in response to hCG was dependent on the LHR, for HCG did not affect [Ca2+]i in L cells not expressing the LHR. The effect was not due to the cAMP-forming activity of the LH receptor, for neither forskolin nor prostaglandin E1, which both increase cAMP levels in L cells, had a similar effect in either control or LHR-expressing cells and isoproterenol had no effect in L cells expressing a functionally active hamster beta-adrenergic receptor. The effect was also not due to overexpression of a Gs-coupled receptor, for L cells expressing 8-fold higher levels of the human V2 vasopressin receptor did not mimic the Ca(2+)-mobilizing response of the LH receptor. We conclude that the LH receptor has the capability of activating two intracellular signaling pathways: one leading to stimulation of adenylyl cyclase and resulting in increases in cAMP and a second leading to stimulation of phospholipase C and resulting in formation of inositol phosphates and elevations in [Ca2+]i. These data correlate positively with and provide a mechanistic explanation for previous reports on the ability of hCG to mobilize phosphoinositides and increasing [Ca2+]i in luteal and granulosa cells (e.g. Davis, J. S., West, L. A., and Farese, R. V. (1984) J. Biol. Chem. 259, 15028-15034).
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PMID:Evidence for dual coupling of the murine luteinizing hormone receptor to adenylyl cyclase and phosphoinositide breakdown and Ca2+ mobilization. Studies with the cloned murine luteinizing hormone receptor expressed in L cells. 131 10

We have investigated synthesis of 3-phosphorylated inositol lipids in growth factor-stimulated Swiss 3T3 cells. Those growth factors tested which act via tyrosine kinase-containing receptors (platelet-derived growth factor (PDGF), insulin growth factor I (IGF-I), epidermal growth factor (EGF), and basic fibroblast growth factor (bFGF)) caused the rapid synthesis of [32P]PtdIns(3,4)P2 and [32P]PtdIns(3,4,5)P3 (PtdIns is phosphatidylinositol) in [32P]P(i)-prelabeled cells and the appearance of an inositol lipid 3-OH kinase in antiphosphotyrosine immunoprecipates. In contrast, those growth factors tested which act via G-protein-coupled receptors (bombesin, vasopressin, prostaglandin E1) were unable to stimulate either of the above responses. Furthermore, while PDGF was able to increase the formation of PtdIns(3,4)P2 and PtdIns(3,4,5)P3 in streptolysin-permeabilized cells, guanosine 5'-3-(thio)triphosphate and guanyl-5'-yl imidodiphosphate were not. These results suggest that Swiss 3T3 cells possess the machinery for tyrosine kinase but not G-protein-mediated activation of PtdIns(4,5)P2 3-OH kinase; a situation which is the inverse to that recently described for human neutrophils. The tyrosine kinase-containing receptors differed markedly in their relative abilities to elevate the levels of [32P] PtdIns(3,4,5)P3 (ranked in the order PDGF greater than or equal to IGF-I greater than EGF greater than bFGF), [32P]Ptd-OH (PDGF greater than EGF greater than bFGF; undetectable for IGF-I), and [32P]PtdIns4P (EGF greater than bFGF greater than PDGF; undetectable for IGF-I) in [32P]P(i)-prelabeled cells. These differences are epitomized by IGF-I, which was the joint most powerful stimulus for [32P] PtdIns(3,4,5)P3 formation, but was unable to stimulate a measurable accumulation of [32P]Ptd-OH (and hence, by deduction, was unable to stimulate phospholipase C). These results indicate that there is a differential ability among the tyrosine kinase-containing receptors present in a single cell to recruit phospholipase C and PtdIns(4,5)P2 3-OH kinase into their signalling complexes and further emphasizes the notion that the rapid synthesis of PtdIns(3,4,5)P3 may be a signalling event.
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PMID:Receptor specificity of growth factor-stimulated synthesis of 3-phosphorylated inositol lipids in Swiss 3T3 cells. 132 11

Three main pathways have been implicated in desensitization of receptors that stimulate adenylylcyclase (AC): cAMP-mediated phosphorylation; cAMP-independent phosphorylation, and receptor internalization. Cell lines derived from the murine Ltk- cell were found useful in exploring the contribution of cAMP-dependent phosphorylation in V2 vasopressin receptor desensitization. The HTB-2 cell expresses the human V2 vasopressin receptor, introduced by transfection of human genomic DNA, and the prostaglandin E1 (PGE1) receptor, endogenous to the Ltk- cell. The A7 cell expresses the hamster beta 2-adrenoceptor, which undergoes the above-mentioned desensitization processes. Treatment of HTB-2 cells with arginine-vasopressin (AVP) had no effect on AC responsiveness to PGE1, but promoted desensitization of the AVP response. This was seen as a 5-6-fold right shift in the dose-response curves for AVP action (cAMP accumulation in intact cells and AC stimulation in homogenates and isolated membranes) and in a decrease in the maximum effect of AVP on these parameters. AVP treatment caused a decrease in cell surface receptors to approximately 75% of control without changes in KD, as determined by Scatchard analysis. When cAMP was increased by treatment with 10 microM PGE1 and isobutylmethylxanthine, desensitization of the PGE1 receptor was observed but not of the AVP receptor. In A7 cells the same treatment caused, as expected, a 3-fold right shift in the dose-response curve for AC stimulation by isoproterenol, indicating that L cells can mediate heterologous desensitization. These data demonstrate that the V2 vasopressin and the PGE1 receptors undergo homologous desensitization in the absence of cAMP-mediated phosphorylation and that this component is not required for vasopressin receptor internalization.
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PMID:Desensitization of the human V2 vasopressin receptor. Homologous effects in the absence of heterologous desensitization. 137 12

Experiments were undertaken to characterize a possible receptor mediating antipyretic action of arginine vasopressin (AVP) within the medial amygdaloid nucleus (meA) in the conscious rat. Additional experiments were directed at determining whether the action of endogenously released AVP can be revealed in the meA during fever in the conscious rat. These objectives were achieved using vasopressin analogues directed against vasopressor (V1a) and antidiuretic (V2) receptors. Bilateral injection of AVP (40 pmol) into the meA of conscious rats suppressed fever evoked by intracerebroventricular (icv) administration of prostaglandin E1 (PGE1, 50 ng). The V2 receptor agonist 1-desamino-8-D-AVP (40 pmol) injected into the meA evoked only moderate antipyresis compared with AVP, possibly because of interaction of this agonist with V1a receptors. The antipyretic effect of AVP was blocked when injection of the peptide was preceded by a bilateral injection of the V1a antagonist 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine AVP [d(CH2)5Tyr(Me)AVP, 400 pmol] into the meA. Injection of d(CH2)5Tyr(Me)AVP alone into the meA was without significant effect on afebrile core temperature. Injection of d(CH2)5Tyr(Me)AVP or 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-D-valine,4-valine AVP (a V2 antagonist) alone into the meA before icv PGE1 resulted in fevers that were not significantly different from artificial cerebrospinal fluid controls. These data are consistent with the possibility that AVP might act within the meA to evoke antipyresis via receptors that resemble V1a (vasopressor) receptors. However, the action of AVP endogenously released into the meA does not appear to be an absolute requisite in the normal modulation of PGE1 fever.
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PMID:Vasopressin-induced antipyresis in the medial amygdaloid nucleus of conscious rats. 153 8

The purpose of the present investigation was to test the hypothesis that drug-induced changes in rumen contractions influence feed intake in dwarf goats. Intravenous (i.v.) administration of clonidine (1 microgram kg-1 min-1 for 10 min), xylazine (1 microgram kg-1 min-1 for 10 min), and PGF-2 alpha (10 micrograms kg-1 min-1 for 15 min) caused bradycardia and inhibition of rumen contractions. However, no appetite-stimulating effect of these drugs was observed. Other clinical changes induced by the alpha-adrenergic agonists included slight sedation and a decrease in body temperature; all clinical effects of clonidine and xylazine were partly antagonized by tolazoline pretreatment (10 micrograms kg-1 min-1 for 30 min). These results suggest that the CNS control of feeding differs in ruminants and monogastric species. In dwarf goats fasted for 2 h, i.v. administration of oxytocin (0.01 IU kg-1 min-1 for 15 min), vasopressin (0.01 IU kg-1 min-1 for 15 min), octapressin (0.003 IU kg-1 min-1 for 15 min) or PGE1 (0.8 microgram kg-1 min-1 for 15 min) did not change feeding behaviour during the two observation periods (0-30 min and 180-210 min after drug infusion, respectively). In previous studies, similar doses of these drugs induced changes in heart rate and inhibition of rumen contraction in goats. These findings demonstrate that drug-induced changes in forestomach contractions do not simply cause changes in feeding behaviour. The i.v. infusion of the PGF 2 alpha analogues etiproston (10 micrograms kg-1 min-1 for 15 min), luprostiol (30 micrograms kg-1 min-1 for 15 min), cloprostenol (1 microgram kg-1 min-1 for 15 min) and tiaprost (1 microgram kg-1 min-1 for 15 min) induced hypophagic effects and stimulated intestinal propulsion.
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PMID:Feed intake and rumen motility in dwarf goats. Effects of some alpha 2-adrenergic agonists, prostaglandins and posterior pituitary hormones. 167 5

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