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

The well-known phenomenon of hangover after ingestion of alcoholic beverages is reviewed; it appears to be due to both ethanol and congeners. Detailed studies must be preceded by the development of a system for measurement of hangover symptoms. Hangover scales are described for measurement of intensity in studies of its drug treatment. Attention is drawn to the changes in hormone levels, notably of aldosterone, renin, cortisol and testosterone in males during hangover.
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PMID:The manifestations, aetiology and assessment of ethanol-induced hangover. 36 Apr 39

The effect of ethanol intoxication and hangover on plasma renin activity (PRA), plasma aldosterone (PA) and plasma cortisol (PC) concentrations was studied in 7 healthy supine men in controlled clinical conditions during 18 h beginning at 6 p.m. Large individual variation was observed in the response of PRA, PA and PC to ethanol. Following ethanol, stimulation of PRA was observed at the 14th and the 16th hour (P less than 0.05), of PA at the 4th and the 6th hour (P less than 0.01 and P less than 0.05, respectively) and of PC at the 4th and the 14th hour (P less than 0.01 and P less than 0.05, respectively). Ethanol ingestion suppressed PC during the first hour (P less than 0.02). Water ingestion at 8 a.m. suppressed PA between the 14th and the 16th hour (8-10 a.m.) in control and ethanol experiment (P less than 0.01 and P less than 0.005, respectively). There was a dissociation between PRA and PA, but intra-individually PRA and PA correlated fairly or well. Plasma arginine vasopressin (AVP) and PC were also significantly correlated. The results suggest that changes in PA and PC as well as the dissociation of PRA and PA after ethanol ingestion might be partly related to dehydration and to the increased secretion of hypothalamic and pituitary hormones as well as to sodium and potassium balance. There was a biphasic effect of ethanol, including an inital suppression of PC and a subsequent increase of PC, PRA and PA. Upright posture appears to exaggerate the stimulating effect of ethanol on PRA, PA and PC.
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PMID:Renin, aldosterone and cortisol during ethanol intoxication and hangover. 46 81

The renin-aldosterone system was studied in human volunteers during ethanol intoxication and hangover. Plasma renin activity increased more than 100%, when 1.5 - 2.3 g ethanol per kg body weight was ingested over a three hour period. During hangover the increase even exceeded 200%. Plasma aldosterone concentration decreased during ethanol intoxication, but increased greatly during hangover. It is suggested that the stimulation of the renin-aldosterone axis during ethanol intoxication and hangover is due to dehydration and increased activity of the sympathetic nervous system.
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PMID:Renin-aldosterone axis in ethanol intoxication and hangover. 126 87

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84