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)

Chronic ethanol administration causes hypertension and alterations of vascular reactivity in rats. In several models of hypertension, alterations of vascular reactivity are believed to be secondary to the sustained increase in blood pressure. The present study investigated the effects of serotonin (5-hydroxytryptamine [5-HT]), vasopressin and acetylcholine (ACh) in the isolated perfused mesenteric arteries from Wistar rats submitted to an 8-week course of chronic ethanol intake (8 g/kg.day). No significant differences were observed in the dose-response curves with regard to: pressor effect of 0.04-10.0 nmole 5-HT; relaxant effect of 0.05-50.0 nmole ACh; or the pressor effects of two 1.5-nmole doses of vasopressin between control rats and ethanol-fed rats. These results suggest that modifications in arterial reactivity to endogenous vasoactive substances (observed in other studies involving more prolonged ethanol treatment in rats) may be, in part, secondary to the increase in blood pressure.
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PMID:Effect of high ethanol intake on vascular reactivity to serotonin, vasopressin and acetylcholine in normotensive rats. 829 56

Previously we reported that 5 min after intracerebroventricular (i.c.v.) injection, serotonin (5-HT, 2.5 micrograms) produced increases in blood pressure and decreases in heart rate in conscious rats that were blocked by LY 53857 (a selective 5-HT2/1C antagonist) and were sensitive to vasopressin antagonism. The present studies were performed to determine if this dose of 5-HT acts similarly to increase plasma vasopressin levels. In addition, the vasopressin responses were compared to prolactin, corticosterone, and plasma renin activity, three other neuroendocrine systems regulated in part by 5-HT. The administration of 5-HT (2.5 micrograms i.c.v.) produced a rapid (maximum response in less than 5 min) and brief (return to baseline by 15 min) increase in plasma vasopressin levels. The response was eliminated by the centrally acting 5-HT2/1C antagonist LY 53857 (100 micrograms/kg i.v.), but only attenuated by xylamidine (100 micrograms/kg i.v.), a 5-HT2/1C antagonist that reportedly does not cross the blood-brain barrier. 5-HT also increased plasma prolactin and corticosterone levels, but neither LY 53857 nor xylamidine altered these responses. In rats rendered chronically baroreceptor deficient by sinoaortic deafferentation, the vasopressin response to 5-HT was reduced, whereas the prolactin response was normal. 5-HT did not increase plasma renin activity in intact or baroreceptor-deficient rats, in contrast to the other neuroendocrine systems studied. Thus, the data demonstrate that vasopressin levels are elevated briefly following 5-HT i.c.v., consistent with the pharmacologic profile of the early cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of serotonin on vasopressin release: a comparison to corticosterone, prolactin and renin. 832 22

Freshly drawn blood samples from seven female and seven male healthy donors were used. Arginine8-vasopressin (AVP) effects on platelet aggregation and serotonin (5-HT) release were examined in adenosine-depleted platelet-rich plasma (PRP) and PRP containing normal amounts of plasma adenosine. No significant differences in the plasma adenosine levels were noted between female (208 +/- 90 nM) and male (239 +/- 85 nM) subjects, but significant differences in AVP-induced platelet aggregation and 5-HT release were noted between female and male subjects. In adenosine-depleted PRP, platelets from most female donors could be aggregated irreversibly at low levels of AVP (18 mU/ml, or 42 nM), whereas platelets from most male donors responded poorly and caused only reversible aggregation at much higher AVP levels (108-720 mU/ml PRP or 252-1,680 nM). In contrast, in PRP containing normal amounts of adenosine, AVP response to induce platelet aggregation was much weaker, demonstrating that adenosine acts as a natural modulator of AVP actions. Theophylline and a relatively selective A2 antagonist DMPX (3,7-dimethyl-1-propargylxanthine) attenuate the plasma adenosine effects causing potentiation in AVP activity on platelet aggregation. These studies suggest that agents that can increase plasma adenosine levels (e.g., inhibitors of nucleoside transport and adenosine deaminase), or adenosine receptor antagonists, may have potential therapeutic uses in modulation of AVP actions in the body. Furthermore, the human platelet serves as a suitable pharmacologic model to study interactions between biologically produced adenosine and AVP.
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PMID:Modulation of vasopressin actions on human platelets by plasma adenosine and theophylline: gender differences. 833 6

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

(+/-)-SDZ NVI 085 (3,4,4a,5,10,10a-hexahydro-6-methoxy-4-methyl-9- methylthio-2H-naphth [2,3-b]-1,4-oxazine hydrochloride), an alpha 1-adrenoceptor agonist, produced a concentration-dependent relaxation (pIC50 of 7.2 +/- 0.1) in the isolated caudal artery of rat precontracted with serotonin (5-hydroxytryptamine, 5-HT, 1 microM). (+/-)- SDZ NVI 085 had no effect upon caudal arteries precontracted with vasopressin or U46619 (9,11-dideoxy-11 alpha, 9 alpha-epoxymethano-prostaglandin F2 alpha). In other studies, (+/-)-SDZ NVI 085 shifted 5-HT concentration-effect curves to the right, in a concentration-dependent manner, and Schild regression gave a pA2 estimate of 8.0 (slope of 1.0). Experiments using pharmacological resultant analysis indicated a syntopic interaction of (+/-)-SDZ NVI 085 with ketanserin (a 5-HT2 receptor antagonist) toward 5-HT-induced contractions. It is concluded that (+/-)-SDZ NVI 085 behaves as a reversible competitive 5-HT2A receptor antagonist, a property which may be of importance regarding its pharmacological effects in vivo.
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PMID:SDZ NVI 085, an alpha 1A-adrenoceptor agonist with 5-HT2A receptor antagonist properties. 885 Nov 70

The present studies investigated the mechanisms mediating the cardiovascular changes induced by intracerebroventricular injection of serotonin (5-HT; 100 nmol) in conscious rats. At 5 min after 5-HT injection, arterial pressure and plasma levels of epinephrine were elevated and heart rate was reduced. The pressor response was abolished either by bilateral adrenalectomy or by pretreatment with chlorisondamine plus vasopressin V1 receptor antagonist. The bradycardic response was attenuated by pretreatment with chlorisondamine or a combination of methylatropine, propranolol, and vasopressin V1 receptor antagonist. At 20 min postinjection, arterial pressure and heart rate were both decreased. The reduction of heart rate at this time point was not blocked by the following pretreatments given alone or in combination: methylatropine, propranolol, vasopressin V1 and V2 receptor antagonists, adenosine A1 receptor antagonist, angiotensin-converting enzyme inhibitor, and chlorisondamine. These results suggest that immediately after intracerebroventricular injection of 5-HT, arterial pressure is elevated through the release of epinephrine and vasopressin and that heart rate is reduced via reciprocal changes in cardiac parasympathetic and sympathetic tone. In contrast, adrenergic, cholinergic, vasopressinergic, purinergic, and angiotensinergic mechanisms do not mediate the bradycardia observed at 20 min postinjection.
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PMID:CNS actions of serotonin on cardiovascular function: nonadrenergic, noncholinergic mechanisms. 885 77

5-Hydroxytryptamine-1A (5-HT1A) receptor agonists, including flesinoxan, reduce anxiety and activate the hypothalamus-pituitary-adrenal (HPA) axis under basal conditions. In order to investigate the underlying neural mechanisms we investigated immunoreactivity for the immediate early gene protein product Fos (Fos-ir) in rat brains 1 h after flesinoxan treatment (0.0, 0.3 or 3.0 mg/kg p.o.). Typically, 5-HT1A receptor-containing brain areas, such as the dorsal raphe nuclei, hippocampus, septum, diagonal band and the cortical and basomedial amygdala, do not show Fos-ir. Apparently, binding of flesinoxan at the 5-HT1A receptor does not directly lead to activation of c-fos in the cell, probably due to its negative coupling to adenylate cyclase. However, in typically non-5HT1A receptor-containing brain areas Fos-ir is increased due to flesinoxan treatment, as in the paraventricular nucleus of the hypothalamus (PVN), the dorsolateral part of the bed nucleus of the stria terminalis (BNSTdl) and the central amygdala (CeA). Flesinoxan-treated rats also exhibited higher plasma corticosterone levels than vehicle-treated animals, which suggests the involvement of corticotropin-releasing hormone (CRH) or vasopressin in the hypothalamus. After double immunolabelling (Fos/CRH or Fos/vasopressin), every CRH neuron detected in the PVN also contained Fos. Moreover, a significant correlation existed between the number of Fos-ir neurons in the PVN and the plasma corticosterone level. Hardly any Fos/vasopressin double labelling was visible in the PVN. Accordingly, flesinoxan exerts its activating effects on the HPA axis via CRH neurons in the PVN. These effects are trans-synaptically mediated by other brain areas, such as the CeA and BNSTdl, which also show increased Fos-ir.
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PMID:5-HT1A receptor agonist flesinoxan enhances Fos immunoreactivity in rat central amygdala, bed nucleus of the stria terminalis and hypothalamus. 895 98

Serotonin (5-hydroxytryptamine, 5-HT)-releasing drugs are important experimental tools to examine the role of serotonergic nerve terminals in the secretion of hormones. The drugs 1-(1,3-benzodioxol-5-yl)-2-(methylamino)butane (MBDB), 5-methoxy-6-methyl-2-aminoindan (MMAI) and p-methylthioamphetamine (MTA) have been suggested to be 5-HT releasers. The present study characterized MBDB, MMAI and MTA by using their effects on the secretion of the hormones adrenal corticotrophin (ACTH), corticosterone, prolactin, oxytocin and renin. The time course of the effect of MBDB, MMAI and MTA (5 mg/kg, i.p.) showed that the peak effect on plasma ACTH occurred 10 min after the injection, whereas the prolactin response did not reach a maximum until 30 min after injection. MBDB increased plasma renin concentration within 10 min, whereas the effect of MTA was significant only at 30 min after injection. All three 5-HT releasers decreased HR (within 5 min) and blood pressure (at 15 min after injection). MBDB, MMAI and MTA increased plasma ACTH, corticosterone, prolactin and renin levels in a dose-dependent manner, whereas no changes were observed in plasma vasopressin concentrations. MTA and MMAI, but not MBDB, significantly increased plasma oxytocin concentrations in a dose-dependent manner. Pretreatment of rats with fluoxetine blocked the ACTH response to MBDB and MMAI, but not to MTA. The prolactin response to all three 5-HT releasers was blocked by fluoxetine. The oxytocin response to MTA and MMAI was inhibited by fluoxetine. The renin responses to all three 5-HT releasers were not significantly inhibited by fluoxetine. The results suggest that MBDB, MMAI and MTA can increase the secretion of several hormones, at least in part, through stimulation of serotonergic neurotransmission. However, these three 5-HT releasers seem to have effects on other (and as yet uncharacterized) mechanisms that can stimulate the secretion of some hormones.
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PMID:Neuroendocrine pharmacology of three serotonin releasers: 1-(1,3-benzodioxol-5-yl)-2-(methylamino)butane (MBDB), 5-methoxy-6-methyl-2-aminoindan (MMAi) and p-methylthioamphetamine (MTA). 896 49

Alterations of the endothelium may play a role in the generation of cerebral vasospasm. The objective of this study was to investigate the involvement of the endothelium and of endogenous endothelin (ET) on the NG-nitro-L-arginine (L-NOARG)-induced contractions in isolated rat basilar arteries. L-NOARG, NG-nitro-L-arginine methyl esther, and methylene blue, but not D-NOARG, induced concentration-dependent contractions and spontaneous vasomotion. The effect of L-NOARG was reversed by L-arginine and submaximally reduced in de-endothelialized arteries. The contractile effect of L-NOARG was completely suppressed by the ET-antagonists BQ 123 and Ro 46-2005 in a part of the basilar arteries. After washout of the respective antagonist, the L-NOARG-induced contraction started, but was not influenced by a second application of the antagonist. In another part of preparations the antagonists failed to influence the L-NOARG-induced contraction. Inconsistent suppressor effects were also observed after preincubation with ketanserin, Manning compound, losartan, or indomethacin. None of these antagonists reversed the established L-NOARG-induced contraction. Thus, endothelium-derived NO suppresses spontaneous contraction and vasomotion in rat basilar arteries. Endogenous ET, 5-HT, vasopressin, angiotensin or cyclooxygenase metabolites do not cause the contraction induced by inhibition of the NO synthase, but may act as 'trigger factors', that may play a role in rat models of cerebral vasospasm or infarction.
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PMID:Contractions induced by NO synthase inhibition in isolated rat basilar artery: role of the endothelium and endogenous vasoconstrictors. 947 Nov 5

In the present study, we examined denervation-induced changes in the sensitivity of hypothalamic postsynaptic serotonin1A (5-HT1A) receptor function with respect to changes in the dose-dependent elevation in plasma hormones [adrenocorticotropic hormone (ACTH), corticosterone, prolactin, oxytocin, prolactin, renin and vasopressin] by the 5-HT1A agonist 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT). Rats received intracerebroventricular (i.c.v.) injections of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or vehicle (0.1% ascorbate in saline) 3 weeks before challenge with increasing doses of 8-OH-DPAT (0, 10, 50 or 200 micrograms/kg s.c.). The effectiveness of 5,7-DHT-induced destruction of serotonergic neurons was confirmed by a 93% reduction in [3H]paroxetine-labeled 5-HT uptake sites in the hypothalamus. No changes in basal levels of ACTH, corticosterone, oxytocin, prolactin, renin and vasopressin were observed in rats that received i.c.v. 5,7-DHT injections. The dose-response curves for 8-OH-DPAT-induced elevations of plasma corticosterone and prolactin levels were shifted to the left in rats treated with 5,7-DHT, whereas no significant difference in the ACTH dose-response curve was observed between rats treated with vehicle and rats treated with 5,7-DHT. In contrast, the maximal oxytocin response to 8-OH-DPAT was attenuated in rats treated with 5,7-DHT. A 5,7-DHT-induced decline in the synthesis of oxytocin could explain this phenomenon. Although 8-OH-DPAT did not increase plasma levels of renin or vasopressin in rats treated with vehicle, 8-OH-DPAT produced an elevation (75%) in plasma renin concentration but not in vasopressin levels in rats that received i.c.v. injections of 5,7-DHT. No change was observed in [3H]8-OH-DPAT labeled 5-HT1A receptors in the hypothalamus. In summary, denervation of hypothalamic serotonergic nerve terminals produces supersensitivity of some neuroendocrine responses to 8-OH-DPAT independent of changes in the density of hypothalamic 5-HT1A receptors.
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PMID:Alterations in 8-hydroxy-2-(dipropylamino)tetralin-induced neuroendocrine responses after 5,7-dihydroxytryptamine-induced denervation of serotonergic neurons. 965 67


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