Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal regeneration hypertension [ARH] was induced after Ingle and Higgins, and Skelton in 13 female Wistar rats one and a half months old with the purpose of studying the function of the renal and the brain renin-angiotensin systems in that model of hypertension, before and after treatment with antihypertensive prostaglandin EI [PGEI]. It was found that a 30 days' application of PGEI induced a regression of the regenerated adrenal cortex, accompanied by a significant decrease in arterial blood pressure to normotensive values. Plasma renin activity did not correlate with the level of the blood pressure nor with kidney renin activity and was not influenced by PGEI. However renal renin activity, which was found to be increased, corresponded to the elevated blood pressure, and decreased almost to normal values with normalization of the blood pressure. A correlation between the brain and kidney renin systems was established in that increased renal renin activity was accompanied by low brain stem and medulla renin activity. The balance was restored by PGEI, which not only lowered blood pressure and decreased renal rein acitivity, but induced an increase of brain stem and medulla renin activity. It is concluded that there exists a notable connection between adrenal cortex regeneration, renal antihypertensive prostaglandins and the kidney and brain renin-angiotensin systems, which pays a correlated role in the mechanism of adrenal regeneration hypertension.
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PMID:The renin-angiotensin systems in adrenal-regeneration hypertension. 102 7

The adrenocortical tissue which regenerates after adrenal enucleation, and contralateral uninephrectomy and adrenalectomy, resembles histologically zona fasciculata tissue which normally synthesises glucocorticoids. However, increases in blood pressure after enucleation (adrenal regeneration hypertension-ARH] were preceded by a rise in exchangeable body sodium similar to that found with mineralocorticoid-induced hypertension (e.g. DOC/salt rat model). Glucocorticoid involvement in ARH rats was tested, firstly by infusing dexamethasone into control and ARH rats to see whether ACTH suppression would lower blood pressure by reducing adrenocortical activity and, secondly, by infusing dexamethasone into rats with intact adrenals to see whether conditions for ARH (i.e. uninephrectomy and/or saline consumption) pre-disposed rats to the hypertensinogenic properties of glucocorticoids. Low-dose dexamethasone infusions (10 micrograms/day for 5 days) in ARH rats did not affect blood pressure but in control animals caused a significant (P less than 0.01) increase from 128 +/- 3 to 151 +/- 5 mmHg. Corticosterone, 18-hydroxycorticosterone and deoxycorticosterone plasma concentrations were suppressed in both groups by dexamethasone treatment; plasma renin concentrations were lower in ARH rats than in controls. Uninephrectomy or 1% NaCl as drinking fluid did not affect the blood pressure rise induced by sc infusion of 10 micrograms dexamethasone/day for 14 days in rats with intact adrenals. The temporal relationship between blood pressure changes and exchangeable body sodium in ARH rats resembles that in mineralocorticoid-induced hypertension. Glucocorticoid, unlike mineralocorticoid, induced hypertension is not affected by a reduction in renal mass or increased sodium intake.
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PMID:The relative importance of glucocorticoids and mineralocorticoids in the development of adrenal regeneration hypertension in rats. 301 53