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)

The activation of the 11-hydroxycorticosteroids secretion by 5-hydroxytryptophan was confirmed in intact rats as well as in those with isolated mediobasal hypothalamus. Deafferentation of the medial basal hypothalamus did not prevent an increase of corticoliberin and vasopressin content in the external median eminence after adrenalectomy and led to an opposite response after 5-hydroxytryptophan injection in these rats. The activation of the vasopressinergic cells and increase of portal vessels' lumen occurred under the 5-hydroxytryptophan effect, particularly in rats subjected to deafferentation combined with adrenalectomy.
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PMID:[The effect of serotonin on the hypothalamic structures that participate in the regulation of the hypophyseal-adrenal cortex system]. 216 65

Deafferentation of sinoaortic baroreceptors produces a marked increase in the lability of arterial pressure that is sustained chronically. Studies reviewed in this paper were designed to determine the mechanisms responsible for generating arterial pressure lability. Pharmacological interruption of the humoral vasopressin and angiotensin systems failed to alter arterial pressure lability. In contrast, blockade of sympathetic nervous system transmission at both ganglionic and alpha-adrenergic receptor levels significantly attenuated lability. A similar effect was observed with the peripheral neurotoxin, 6-hydroxydopamine. After blockade of sympathetic transmission, a further reduction in lability was produced by blocking the renin-angiotensin or vasopressin systems. The dissociation of the level of arterial pressure from lability was achieved with parachloroamphetamine which raised arterial pressure but reduced lability. A substantial peripheral contribution to lability was obtained in experiments in which the alpha-adrenergic agonist, phenylephrine, produced a marked increase in lability in both normal and baroreceptor-denervated animals in which humoral and neural transmission were blocked. These data demonstrate that following baroreceptor deafferentation, arterial pressure lability is produced primarily by the sympathetic nervous system and secondarily by circulating humoral factors that appear to act on vascular smooth muscle to induce fluctuations in the level of arterial pressure.
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PMID:Central and peripheral mechanisms of arterial pressure lability following baroreceptor denervation. 312 Nov 55