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)

Production, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the specific protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gamma-aminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considred. Serotonin, dopamine and taurine, however, may not be involded in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a "readily-releasable pool" of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.
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PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

In order to study the action of serotonin (5-HT), noradrenaline (NA), hypertensin (HT), prostaglandins A1, B1 and E2 (PGA1, PGB1 and PGE2) and vasopressin (VP), internal carotid arteries were isolated in situ from both cerebral and general circulation and perfused continuously with oxygenated Ringers' bicarbonate solution. The order of potencies of the vasoactive substances when administered intra-arterially was: 5-HT greater than HT greater than PGE2- greater than PGB1 greater than NA. The relative duration of the constrictor effects was: 5-HT less than PGA1-less than HT and PGE2 less than PGB1 and NA less than VP. The relaxation index of these substances on the vascular wall was: 5-HT less than PGE2 less than HT less than PGB1-less than NA less than PGA1 less than VP. Some of these substances, specifically PGB1, PGE2 and VP, frequently caused a residual constriction of the smooth muscle following their dilator effect. The role of these vasoactive substances in the development of vasospasm is discussed.
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PMID:Responses of the internal carotid artery to different endogenous vasoconstrictor substances. 44 76

In order to study the control of vasopressin-release, the effect of a series of potential agents was studied in an in vitro perifusion system of rat neurohypophysis after in vivo treatment with nialamide, a monoamine oxidase inhibitor. In this system, metlatonin stimulated vasopressin-release in a dose-dependent manner (1 x 10-8 to 1 x 10-3 M). Serotonin (1 x 10-3 M) also led to a significant increase of vasopressin-release whereas quipazine (1 x 10-3 M), a putative serotonin agonist and monoamine oxidase inhibitor, caused a 3-fold stimulation of the release of the neurohormone. The stimulatory effects of melatonin and serotonin were prevented by omission of Ca2+ combined to an excess of Mg2+ (12mM) in the perifusion medium. 1 x 10-6 M somatostatin did not affect basal or melatonin-stimulated vasopressin-release. These results show that melatonin and serotonin can have a direct stimulatory effect on vasopressin release at the neurohypophyseal level.
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PMID:Melatonin-and serotonin-stimulated release of vasopressin from rat neurohypophysis in vitro. 46 80

The influence of substances known as low molecular weight mediators such as biogenic amines, peptides and prostaglandins on the plasminogen activator release was studied in the isolated perfused pig ear. Among the substances tested, histamine and the plasma kinins bradykinin and kallidin were found to possess a dose-dependent activator-releasing effect, which in case of histamine can be suppressed by an antihistamine (promethazine). Serotonin and the prostaglandins at concentrations up to 10(-5)M possess no significant activator-releasing effect. Compared with the biogenic peptides angiotensin, oxytocin, vasopressin, and eledoisin, only the latter was found to release plasminogen activator. Studies on the influence of the substances tested on the capillary permeability showed that enhanced permeability is caused only by those mediators which cause also increased activator release.
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PMID:[Influence of mediators on plasminogen activator release]. 75 12

This study was undertaken to examine whether several of the hormones that can be released by activation of serotonin receptors will be affected by long-term cocaine administration. Male rats received cocaine injections (15 mg/kg, IP) twice daily for 7 days. Forty-two hr after the last cocaine injection, the rats were challenged with increasing doses (0, 1, 5, 10 mg/kg, IP) of the 5-HT1/5-HT2 agonist MK-212 (6-chloro-2-[1-piper-azinyl]-pyrazine). The following observations were made: (1) cocaine reduced the rate of body weight gain; (2) cocaine inhibited the stimulatory effect of MK-212 on plasma vasopressin, oxytocin, and prolactin concentrations and on plasma renin activity and concentration; (3) cocaine did not inhibit the stimulatory effect of MK-212 on plasma ACTH or corticosterone concentrations. The data indicate that a wide-spectrum 5-HT (serotonin) agonist such as MK-212 can reveal differential neuroendocrine responses. This effect could be related to cocaine-induced changes in the different 5-HT receptor subtypes that regulate the secretion of these hormones.
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PMID:Effect of cocaine injections on the neuroendocrine response to the serotonin agonist MK-212. 133 9

Several classes of drugs that modify serotonin (5-HT) neurotransmission are either currently used, or are being evaluated for their potential use in the treatment of anxiety, schizophrenia, and depression. 5-HT1A agonists are considered potential anxiolytics, while some atypical antipsychotics are potent 5-HT2 antagonists (and also have modest dopamine D2 affinity). Furthermore, there is a diverse group of serotonergic drugs that may be effective antidepressants. Secretion of ACTH, corticosterone/cortisol, prolactin, renin, oxytocin and vasopressin are stimulated by activation of different 5-HT receptor subtypes, while other neurotransmitter receptors also influence the secretion of these hormones. We compared the receptor binding profiles of 5-HT anxiolytics, antipsychotics and antidepressants with their endocrine effects. These comparisons could aid in understanding both the therapeutic and side effects of these drugs.
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PMID:Endocrine and receptor pharmacology of serotonergic anxiolytics, antipsychotics and antidepressants. 135 27

The vasoconstrictor effect of the peptides neuropeptide Y (NPY), endothelin (ENDO), vasopressin (VPR) and oxytocin (OXY) (10(-11)-10(-7) M) was compared in the isolated basilar (BAS) and mesenteric (MES) arteries of rat. The contractile activity of these peptides was compared to that of three nonpeptidergic constrictors: noradrenaline (NA), serotonin (5-hydroxytryptamine, 5-HT) and prostaglandin F2 alpha (PGF2 alpha) (10(-8)-10(-4) M). As regards EC50 values, PGF2 alpha was equally potent in both vessels studied, 5-HT was more potent in BAS and NA was without contractile effect in BAS. Pronounced regional differences were found for the peptides studied. BAS was more sensitive in EC50 values to the peptides in the order ENDO > or = VRP > OXY > NPY. In MES, OXY and NPY caused no and VPR caused weak contraction, whereas the effect of ENDO was pronounced, with a similar EC50 value as in BAS. In conclusion, marked regional differences were found in response to contractile agents in the vascular beds studied. Peptidergic constrictor mechanisms might be of large importance in the regulation of cerebral blood flow during physiological or pathophysiological conditions.
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PMID:Regional differences in the contractile activity of neuropeptide Y, endothelin, oxytocin and vasopressin: comparison with non-peptidergic constrictors. An in vitro study in the basilar and mesenteric arteries of the rat. 136 91

The CSF is often regarded as merely a mechanical support for the brain, as well as an unspecific sink for waste products from the CNS. New methodology in receptor autoradiography, immunohistochemistry and molecular biology has revealed the presence of many different neuroendocrine substances or their corresponding receptors in the main CSF-forming structure, the choroid plexus. Both older research on the sympathetic nerves and recent studies of peptide neurotransmitters in the choroid plexus support a neurogenic regulation of choroid plexus CSF production and other transport functions. Among the endocrine substances present in blood and CSF, 5-HT, ANP, vasopressin and the IGFs have high receptor concentrations in the choroid plexus and have been shown to influence choroid plexus function. Finally, the choroid plexus produces the growth factor IGF-II and a number of transport proteins, most importantly transthyretin, that might regulate hormone transport from blood to brain. These studies suggest that the choroid plexus-CSF system could constitute an important pathway for neuroendocrine signalling in the brain, although clearcut evidence for such a role is still largely lacking.
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PMID:Neuroendocrine regulatory mechanisms in the choroid plexus-cerebrospinal fluid system. 139 90

The intracerebroventricular (i.c.v.) injection of serotonin (5-HT) increases blood pressure and decreases heart rate (HR) in conscious rats by activation of 5-HT2/1C receptors. Since the bradycardia is eliminated by pretreatment with a ganglionic or V1-vasopressin antagonist, we proposed that the decrease in HR results from an effect on cardiac autonomic activity which is potentiated by vasopressin. The present study aimed first, to further characterize mechanisms by which the i.c.v. injection of 5-HT (2.5 micrograms) decreases HR in conscious rats, and second to determine the cardiovascular responses to 5-HT (2.5 micrograms, i.c.v.) in rats with chronic sinoaortic deafferentation (SAD). In intact rats, the bradycardia elicited by 5-HT was eliminated by a combination of the muscarinic antagonist atropine and the beta-adrenoceptor antagonist sotalol; neither antagonist was effective alone. In rats with SAD, 5-HT produced a larger increase in blood pressure and a marked tachycardia, both of which were eliminated by the 5-HT2/1C antagonist LY 53857. Furthermore, in rats with SAD the 5-HT-induced increase in HR was blocked by sotalol alone. In conclusion, 5-HT (2.5 micrograms, i.c.v.) acts on central 5-HT2/1C receptors to increase arterial pressure. In intact rats this decreases HR by vasopressin-potentiated activation of baroreceptor reflexes and subsequent increase in vagal tone and decrease in cardiac sympathetic tone. In the absence of baroreflexes, a direct central effect of 5-HT to produce a beta-adrenoceptor-mediated cardioacceleration is unmasked.
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PMID:Effects of central serotonin on autonomic control of heart rate in intact and baroreceptor deficient rats. 139 42

1. The effects of intracerebroventricular injections to the right lateral ventricle (i.c.v.) of 5-hydroxytryptamine (5-HT, 40 and 120 nmol kg-1), N,N-di-n-propyl-5-carboxamidotryptamine (DP-5-CT; 3 nmol kg-1), 5-carboxamidotryptamine (5-CT; 3 nmol kg-1), 8-hydroxy-2-(di-N-propylamino) tetralin (8-OH-DPAT; 3, 40 and 120 nmol kg-1) and 1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane (DOI; 40 and 120 nmol kg-1) on renal sympathetic nerve activity, blood pressure, heart rate and phrenic nerve activity were investigated in normotensive rats anaesthetized with alpha-chloralose. 2. 5-HT caused a long lasting pressor response which was associated with an initial bradycardia and renal sympathoinhibition followed by a tachycardia and renal sympathoexcitation. Pretreatment with the 5-HT2/5-HT1C receptor antagonists, cinanserin (300 nmol kg-1, i.c.v.) or LY 53857 (300 nmol kg-1, i.c.v.) reversed the initial bradycardia and sympathoinhibition to tachycardia and sympathoexcitation. Combined pretreatment with LY 53857 (300 nmol kg-1, i.c.v.) and the 5-HT1A antagonist, spiroxatrine (300 nmol kg-1, i.c.v.), blocked the effects of 5-HT on all the above variables. 3. Pretreatment with the vasopressin V1-receptor antagonist, beta-mercapto-beta,beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8-vasopressin [(d(CH2)5Tyr(Me)AVP, 10 micrograms kg-1, i.v.] did not affect the magnitude but reduced the duration of the pressor response produced by i.c.v. 5-HT and reversed the initial bradycardia and renal sympathoinhibition to tachycardia and sympathoexcitation. 4. 1-(2,5-Di-methoxy-4-iodophenyl)-2-aminopropane (DOI) caused a pressor effect which was associated with a bradycardia and sympathoinhibition. These effects were blocked by pretreatment with BWSOlC67 (0.1 mg kg-', i.v.), a peripherally acting 5-HT2/5-HTc receptor antagonist. However,BWSOlC67 (0.1 mg kg-', i.v.) failed to block the effects of i.c.v. 5-HT.5. DP-5-CT, 5-CT and 8-OH-DPAT (3 nmol kg-', i.c.v.) caused sympathoexcitation, tachycardia and a rise in blood pressure. Pretreatment with methiothepin (1 mg kg-', i.v.) or spiroxatrine (300 nmol kg-',i.c.v.) attenuated the response to i.c.v. DP-5-CT.6. It is concluded that i.c.v. administration of 5-HT activates 5-HTlA receptors to cause sympathoexcitation and 5-HT2 or 5-HT1c receptors to cause the release of vasopressin.
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PMID:Central administration of 5-HT activates 5-HT1A receptors to cause sympathoexcitation and 5-HT2/5-HT1C receptors to release vasopressin in anaesthetized rats. 146 25


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