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)

Intrathecal injection of arginine vasopressin in rats at a dose as small as 10 ng produced dose-dependent hypertension and tachycardia. Pretreatment with the ganglionic blocking agent Ecolid, alpha-adrenoceptor antagonist phenoxybenzamine or the monoamine depleting agent reserpine blocked this effect without affecting intravenous vasopressin-induced hypertension. Intracerebroventricular injection of arginine vasopressin also induced hypertension and tachycardia, but 600 ng was needed. Ecolid and phenoxybenzamine also abolished this effect. Reserpine was not tested. It is concluded that both intrathecal and intracerebroventricular vasopressin-induced hypertension appears to be mediated by the sympathetic system and that the spinal cord is more sensitive than the supraspinal sites to vasopressin in regulating autonomic functions.
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PMID:New evidence for neuronal function of vasopressin: sympathetic mediation of intrathecal vasopressin-induced hypertension. 376 34

We measured [3H]prolactin ([3H]Prl) synthesis and secretion in female rat anterior hemipituitary glands incubated in vitro, and immunoassayable Prl secretion from dispersed anterior pituitary cells in a perfused column. Anterior pituitary glands which were incubated in 9 microM reserpine showed a marked inhibition of [3H]Prl secretion but no change in hormone synthesis, thus causing [3H]Prl accumulation within the gland. The same concentration of reserpine produced a similar effect in pituitary glands taken from rats depleted of dopamine with alpha-methyl-p-tyrosine. Reserpine inhibited Prl secretion from dispersed anterior pituitary cells with a gradual onset and prolonged duration. Thyrotropin-releasing hormone (TRH), but not dibutyryl cyclic AMP (dbcAMP), the calcium ionophore A23187 or excess Ca2+, stimulated both [3H]Prl and Prl secretion in the presence of reserpine. In contrast, neither basal nor vasopressin-stimulated ACTH (bio- and immunoassayable) secretion was inhibited by 9 microM reserpine. Ultrastructurally, pituitary glands incubated in reserpine had an increased content of Prl secretory granules. Reserpine thus selectively inhibited Prl secretion, secondarily causing accumulation of both measurable hormone and Prl secretory granules within the pituitary gland. We hypothesize that reserpine interrupted calcium-dependent mechanisms in the stimulus-secretion coupling process to inhibit Prl release.
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PMID:Reserpine inhibits rat anterior pituitary hormone secretion in vitro: effects on prolactin and ACTH and ultrastructural observations. 629 87

In the rat hypothalamus, antibodies to ovine CRF41 stain neurons of a paraventriculo-infundibular neuroglandular pathway. CRF like immunoreactivity (CLI)-containing perikarya are mostly packed in the parvocellular division of the paraventricular nucleus. Their morphology and topography differ from that of other peptidergic neurons. However a few CLI perikarya are also stained with vasopressin antibodies. CLI neurons project massively to the external layer of the median eminence (ELME). Adrenalectomy induced a total depletion of ELME CLI 12 to 24 h after surgery, followed by a secondary accumulation already conspicuous 5 days later. This biphasic evolution, identical to that of ELME vasopressin, is totally prevented by a replacement therapy with dexamethasone. Reserpine also induces an acute depletion of ELME CLI and vasopressin, that can be prevented by a monoamine oxidase inhibitor pretreatment. These results indicate the involvement of CLI neurons in the corticotropic axis, suggesting that they are indeed corticoliberin neurons. Among the extrahypothalamic locations of CLI neurons their abundance in the amygdala central nucleus is of interest since it is involved in the corticotropic axis. A similar pattern of CLI was noticed in several mammalian brains and also in lower vertebrates (birds, reptiles, amphibians, fishes). Species adaptations of CLI neurons were observed: CLI neurons are of the cerebrospinal fluid contacting type in the turtle. CLI fibres terminate close to corticotrophs in the fish pituitary. This suggests a direct excitosecretory role of CRF on these cells and concurs with a CRF function of CLI peptide even in fishes. CLI processes and terminals appear in the human fetal ELME at the 16th week of development and increase in number during the following weeks. Perikarya are seen at 19 weeks. In the rat CLI fibers and perikarya were detected as early as the 18th day of fetal development. Thus, paraventriculo-infundibular CLI system develops later than corticotrophs. This chronology perfectly concurs with the results of previous physiological and experimental studies.
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PMID:Corticoliberin neurons: cytophysiology, phylogeny and ontogeny. 636 84

An acute reserpine treatment has the same selective and marked depleting effect on corticoliberin-like immunoreactivity as on vasopressin-like immunoreactivity in the rat zona externa of the median eminence. Somatostatin and gonadoliberin immunoreactivities appear unmodified. Reserpine effect is blocked by pretreatment with monoamine oxidase inhibitors (pargyline or tranylcypromine). Present results support the notion of an inhibitory role of monoamines, particularly catecholamines, on the release of corticoliberin.
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PMID:Reserpine-induced depletion of corticoliberin (CRF)-like immunoreactivity in the zona externa of the rat median eminence. 660 76