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)

gamma-Aminobutyric acid (GABA) has been identified in axon terminals innervating neurons of the supraoptic nucleus and has been shown to inhibit the electrical activity of supraoptic neurons when applied iontophoretically. This study examines the effects of GABA and GABA antagonists on vasopressin (VP) release from organ-cultured explants of the hypothalamo-neurohypophyseal system (HNS). The GABA antagonists bicuculline and picrotoxin stimulated VP release in a concentration-dependent manner. These observations suggest that VP release by HNS explants is tonically inhibited by GABA. Exposure of HNS explants to GABA (10(-8)-10(-3) M) did not consistently alter basal VP release. This was true even when penicillin, which can block GABA-activated chloride channels, was omitted from the medium. Similarly, nipecotic acid, an agent that potentiates GABA activity by inhibiting GABA uptake, did not alter basal VP release; stimulation of VP release by acetylcholine and increases in osmolality was not diminished by the addition of 10(-5) M GABA. The failure of exogenous GABA to modify basal and stimulated VP release suggests that GABAergic inhibition of VP release is maximally activated by endogenously released GABA in cultured HNS explants. This is consistent with evidence for a local source of GABA in the supraoptic nucleus and suggests that one role of GABA in the regulation of VP release is that of a potent local inhibitory neurotransmitter.
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PMID:gamma-Aminobutyric acid antagonists stimulate vasopressin release from organ-cultured hypothalamo-neurohypophyseal explants. 243 37

Immunoreactive galanin-like material was recently shown to co-exist with vasopressin in parvocellular and magnocellular perikarya of the paraventricular nucleus in the anterior hypothalamus of the rat (Melander et al. 1986). Since this distribution pattern differed from our observation of oxytocin-associated galanin-like immunoreactivity (LI) in the neurohypophysis, we compared in series of 0.5-microns thick sections the localisation of galanin-LI with the localisation of oxytocin and vasopressin/dynorphin in the hypothalamus, the median eminence and the neurohypophysis. In the oxytocin system, galanin-LI was intense in oxytocin varicosities of the neurohypophysis. Oxytocin perikarya of the hypothalamic supraoptic and paraventricular nuclei exhibited galanin-LI only after intraventricular injection of colchicine and when sections were treated with trypsin prior to application of the antibody. In the vasopressin/dynorphin system galanin-LI was intense in hypothalamic perikarya after colchicine injection and in neurohypophysial varicosities after treatment of the sections with trypsin. In these neurones, galanin-LI was absent or weak in all elements when treatments with colchicine or trypsin were omitted. Galanin-LI in the neurohypophysis was not co-localised with the numerous fine endings showing GABA-LI. These observations indicate that galanin-like material coexists with vasopressin and oxytocin in the respective magnocellular neurones, although not always in an immunoreactive form.
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PMID:Immunoreactive galanin-like material in magnocellular hypothalamo-neurohypophysial neurones of the rat. 247 16

Administration of diazepam, an agonist of benzodiazepine receptors, and muscimol, an agonist of GABA(A) receptors, resulted in an increase in cytosol GABA-modulin in hypothalamus and cerebellum. Low dose of muscimol, ineffective by itself, completely antagonized the isoniazid, bicuculline and picrotoxin-induced decrease in GABA-modulin activity. In contrast, low dose of diazepam was able to block only the action of isoniazid. That confirms different mechanism of action of muscimol and diazepam. The increase in cytosol GABA-modulin activity in the anterior and posterior hypothalamus of spontaneously hypertensive rats (SHR) and of vasopressin hypertensive rats required much higher doses of muscimol than in normotensive animals showing subsensitivity of GABA(A) receptors in these brain structures. In contrast, the sensitivities of GABA(A) receptors in the cerebellum and of benzodiazepine receptors in the hypothalamus and cerebellum were equal to hypertensive and normotensive rats.
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PMID:The responsiveness of central benzodiazepine and GABA(A) receptors in vasopressin and spontaneously hypertensive rats. 256 66

The GABAergic innervation of vasopressin-containing cells in the magnocellular part of the paraventricular nucleus was studied at the electron-microscope level using antibodies against GABA and vasopressin. The detection of both GABA and vasopressin on the same ultrathin section, performed with a double-labeling immunogold method, revealed GABAergic terminals in symmetrical synaptic contact with vasopressin-containing neurons. These GABAergic terminals displayed mitochondria, clear synaptic vesicles and varying numbers of electron-dense vesicles. Vasopressin-immunoreactivity was associated with neurosecretory granules, whereas GABA-immunoreactivity was found above mitochondria, clear synaptic vesicles and some electron-dense vesicles. This study, demonstrating the extensive participation of GABA in the innervation of magnocellular vasopressin-secreting neurons, suggests that this inhibitory neurotransmitter regulates vasopressin secretion at the level of the paraventricular nucleus.
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PMID:Simultaneous immunogold labeling of GABAergic terminals and vasopressin-containing neurons in the rat paraventricular nucleus. 273 9

The release of oxytocin and vasopressin from rat neurointermediate lobes was determined in vitro. The electrically evoked release of posterior pituitary hormones was markedly potentiated by the GABA receptor agonist, isogauvacin, an effect which was abolished by the GABAA receptor antagonist bicuculline. Spontaneous hormone outflow was not affected by the substances tested. The results suggest the existence of a GABA receptor on the terminal fibres in the pituitary, facilitating the release of oxytocin and vasopressin.
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PMID:GABA receptor stimulation increases the release of vasopressin and oxytocin in vitro. 282 74

Plasma vasopressin (AVP) levels were measured at rest (mean arterial pressure 80-85 mmHg) and during hypotension (mean arterial pressure 38-45 mmHg) induced by ganglionic blockade (trimethaphan) in halothane-anaesthetized respirated rats with end-tidal pCO2 maintained at 34-40 mmHg. Hypotension (15 min) produced a 310% increase in plasma AVP (+/- 60% S.E.M.) which was not reduced significantly by prior baro- and chemoreceptor denervation. The hypotension-induced rise in AVP was blocked by bilateral microinjections (40 nl) of the GABA-mimetic agent muscimol (151 pmol) into the ventrolateral medulla at obex level and significantly attenuated by injections of the same amount in the nucleus tractus solitarius. The rise in AVP was unaffected by microinjections in the pontine locus coeruleus. It was also blocked by bilateral microinjections of the glutamate-receptor antagonist kynurenate (40 nl, 1.8 nmol) into the ventrolateral medulla but unaffected by microinjections of the inactive analogue xanthurenic acid (40 nl, 1.8 nmol). A significantly smaller rise in plasma AVP (88%) was observed following bilateral nephrectomy. It is concluded that, in this preparation, hypotension produces the release of AVP via a mechanism largely independent of baro- and chemoreceptors, which requires the activation of neurones located in the caudal medulla oblongata. The same or closely related neurones may be activated by a neural or hormonal signal generated by the kidney.
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PMID:Baroreceptor-independent medullary mechanism for release of vasopressin during hypotension in rats. 284 27

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

A number of alcohol research groups have measured anterior and posterior pituitary hormones, the endogenous opiates, CNS peptides, and putative neurotransmitters during alcohol withdrawal. The data are often complex and contradictory, though a number of themes have emerged. Activity of the hypothalamic-pituitary-adrenal axis (HPA) is increased during chronic alcohol exposure and appears to remain altered for at least 2 to 4 weeks after cessation of drinking. There is increased turnover of norepinephrine and enhanced binding of CNS adrenergic receptors. By contrast, there are decreases in CNS activity of select endogenous opiates and GABA. Other CNS compounds that may play a role in alcohol withdrawal are prolactin, thyrotropin-releasing hormone (TRH), vasopressin, cyclic 3'5'-adenosine monophophate (cAMP), Delta-sleep-inducing peptide (DSIP), and iron. Despite many studies in humans and animals, the roles of CNS dopamine and serotonin in withdrawal remain unclear. A number of peptides, including cholecystokinin (CCK), neurotensin, and bombesin, have been shown to interact with the CNS actions of alcohol and may play a role in alcohol withdrawal. Inadequate work has been performed on acetylcholine (ACh), human growth hormone (HGH) and luteinizing hormone (LH). Studies of the recently identified GABA-benzodiazepine-barbituate receptor complex indicate that this system is likely to be involved in the pathophysiology of alcohol withdrawal. Perturbation studies with corticotropin-releasing factor (CRF) and TRH (with measures of ACTH and cortisol and TSH and prolactin, respectively), may identify patients with withdrawal-related autonomic dysfunction.
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PMID:Clinical neuroendocrinology and neuropharmacology of alcohol withdrawal. 301 Mar 91

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

1. gamma-Aminobutyric acid (GABA) inhibited the antidiuretic response and the increased urinary excretion of vasopressin produced by carbachol when both drugs were injected into a lateral cerebral ventricle (i.c.v.) in the water-loaded rat under ethanol anaesthesia. 2. The inhibitory effect of GABA was mimicked by muscimol and 3-amino-1-propane sulphonic acid (3-APS) and blocked by bicuculline. 3. GABA injected i.v. or into the cisterna magna (i.cist.) did not inhibit the release of vasopressin by carbachol injected i.c.v. 4. The results suggest a role for GABA as a putative inhibitory transmitter in the hypothalamo-neurohypophysial system, acting directly on the supraoptic or paraventricular nuclei in the anterior hypothalamus.
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PMID:Central inhibition by gamma-aminobutyric acid of the release of vasopressin by carbachol in the rat. 335 7


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