Nieminen M M, Linkola J, Fyhrquist F, Tikkanen I, Forslund T
Int J Clin Pharmacol Ther Toxicol. 1985 Mar;23(3):137-40.
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.
在中度乙醇中毒期间，血浆肾素活性（PRA）升高而血浆醛固酮未升高。为了阐明肾素 - 醛固酮联系解离背后的机制，六名健康男性在摄入乙醇（1.2 g/kg体重）后通过静脉输注给予血管紧张素II（4 ng·kg⁻¹·min⁻¹）。在输注血管紧张素II（A II）之前，PRA升高而血浆醛固酮下降。在乙醇中毒和对照实验中，A II输注均使血浆醛固酮增加约3倍，并使PRA短暂抑制。血浆肾素底物、皮质醇和血管紧张素转换酶（ACE）保持不变。乙醇中毒时血清钾降低或Na⁺/K⁺比值升高可能解释了肾上腺皮质未能对内源性血管紧张素II作出醛固酮释放反应的原因。然而，所输注的A II的升压剂量明显克服了我们之前报道的乙醇对醛固酮释放的抑制作用。在乙醇和对照实验中，响应A II输注时舒张压和收缩压的升高相似，但有一名受试者除外，该受试者在乙醇中毒期间血压出现反常下降，而在无乙醇情况下对A II输注反应正常。
