Renin-aldosterone axis in ethanol intoxication: effect of a Ii infusion
Nieminen, M.M.; Linkola, J.; Fyhrquist, F.; Tikkanen, I.; Forslund, T.
International Journal of Clinical Pharmacology Therapy and Toxicology 23(3): 137-140
1985
ISSN/ISBN: 0174-4879 PMID: 2987138 Document Number: 256425
Plasma renin activity (PRA) is increased while plasma aldosterone is not, during moderate ethanol intoxication. To elucidate mechanisms behind this dissociation of renin-aldosterone nexus, six healthy males were given angiotensin II (4 ng kg-1 min-1) by i.v. infusion following ingestion of ethanol (1.2 g kg-1 body weight). Prior to angiotensin II (A II) infusion, PRA rose and plasma aldosterone declined. A II infusion caused a roughly 3-fold increase of plasma aldosterone both in ethanol intoxication and in control experiments, and a transient suppression of PRA. Plasma renin substrate, cortisol, and angiotensin converting enzyme (ACE) remained unchanged. The decrease of serum potassium or the rise of Na+/K+ ratio in ethanol intoxication may explain the failure of the adrenal cortex to respond with aldosterone release to endogenous angiotensin II. However, the pressor dose of A II infused obviously overcame the blunting effect of ethanol on aldosterone release previously reported by us. Blood pressure, both diastolic and systolic, increased similarly during ethanol and control experiments in response to A II infusion, except in one subject, who during ethanol intoxication experienced a paradoxical fall in blood pressure while reacting normally to A II infusion without ethanol.