Renin-aldosterone axis in ethanol intoxication: effect of A II infusion

Area of Science:

• Endocrinology
• Pharmacology
• Renal Physiology

Background:

• Moderate ethanol intoxication alters the renin-aldosterone system, characterized by increased plasma renin activity (PRA) without a corresponding rise in plasma aldosterone.
• The mechanisms underlying this dissociation between renin and aldosterone during ethanol intoxication are not fully understood.

Purpose of the Study:

• To investigate the mechanisms behind the dissociation of the renin-aldosterone nexus during moderate ethanol intoxication.
• To determine the effect of exogenous angiotensin II (A II) on aldosterone release and PRA in the presence of ethanol.

Main Methods:

• Six healthy males ingested ethanol (1.2 g kg-1 body weight).
• Intravenous infusion of angiotensin II (4 ng kg-1 min-1) was administered.
• Measurements included plasma renin activity, plasma aldosterone, plasma renin substrate, cortisol, angiotensin converting enzyme (ACE), serum potassium, Na+/K+ ratio, and blood pressure.

Main Results:

• Prior to A II infusion, PRA increased and plasma aldosterone decreased during ethanol intoxication.
• A II infusion significantly increased plasma aldosterone approximately threefold in both ethanol-intoxicated and control states, and transiently suppressed PRA.
• Ethanol intoxication led to a decrease in serum potassium and an increase in the Na+/K+ ratio, potentially explaining the blunted aldosterone response to endogenous A II.

Conclusions:

• The pressor dose of infused A II overcame the blunting effect of ethanol on aldosterone release.
• Changes in serum potassium and Na+/K+ ratio during ethanol intoxication may impair the adrenal cortex's aldosterone response to endogenous angiotensin II.
• Blood pressure responses to A II infusion were similar in both ethanol and control conditions, with one exception of a paradoxical fall in blood pressure during ethanol intoxication.