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Effect of Chronic Ethanol Consumption on the Atrial Natriuretic System of Spontaneously Hypertensive Rats
Author(s) -
Guillaume Pascal,
Jankowski Marek,
Gianoulakis Christina,
Gutkowska Jolanta
Publication year - 1996
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1996.tb01712.x
Subject(s) - medicine , atrial natriuretic peptide , endocrinology , vasopressin , peptide hormone , aldosterone , arginine , blood pressure , hormone , chemistry , amino acid , biochemistry
There is a lot of discussion on the effects of ethanol (ETOH) on blood pressure (BP). It has been suggested that chronic moderate ETOH consumption prevents the development of age‐dependent hypertension in humans and spontaneously hypertensive rats (SHR). However, the mechanism mediating this effect is unknown. In the present studies, we hypothesized the implication of atrial natriuretic peptide (ANP), a BP‐lowering hormone, on the antihypertensive effect of moderate ETOH consumption. A 20% v/v solution of alcohol was given as drinking fluid to SHR and normotensive Wistar‐Kyoto (WKY) rats for up to 32 weeks. This treatment prevented, at least in part, the age‐dependent increase of BP in SHR and WKY rats. The lower BP was associated with significantly lower levels of circulating atrial natriuretic peptide in both groups. After chronic ETOH administration, total ANP content and concentration were higher in the left and right atria of SHR and WKY rats than in water‐treated controls. Despite the ETOH‐induced increase in atrial ANP content, there was no significant change in atrial ANP mRNA, suggesting decreased atrial release. Chronic ETOH treatment significantly reduced ANP mRNA in the ventricles of SHR but not of WKY rats. Correspondingly, ventricular ANP content and concentration were lowered by ETOH in SHR only. Chronic ETOH administration induced a significant increase of plasma arginine vasopressin and a significant decrease of plasma aldosterone in SHR but not in WKY rats. Thus, chronic ETOH treatment prevented the age‐dependent elevation of BP in both SHR and WKY rats, and altered the activity of heart ANP as well as of the aldosterone and plasma arginine vasopressin systems.