Lowenstein J, Steele J M
Kidney Int. 1977 Feb;11(2):128-35. doi: 10.1038/ki.1977.18.
The role of the renin-angiotensin system in mediating the aldosterone response to sodium depletion was examined by administration of propranolol during dietary sodium restriction. The beta-adrenergic antagonist prevented the expected increase of plasma renin activity in response to sodium restriction in six of twelve studies. Plasma angiotensin II concentration failed to increase in four of five subjects in whom the renin response was abolished. Despite unchanged or decreased plasma renin activity and plasma angiotensin II concentration, plasma aldosterone concentration increased significantly in response to dietary sodium restriction. The increase in aldosterone production could not be attributed to changes in plasma sodium or potassium concentration or increased ACTH secretion. It is suggested that the aldosterone response to sodium restriction is mediated not only by increased plasma renin activity and angiotensin II concentration, but also another mechanism, possibly related to increased adrenal sensitivity to angiotensin during sodium depletion.
通过在饮食钠限制期间给予普萘洛尔,研究了肾素 - 血管紧张素系统在介导醛固酮对钠耗竭反应中的作用。在十二项研究中的六项中,β-肾上腺素能拮抗剂阻止了因钠限制而预期的血浆肾素活性增加。在五项肾素反应被消除的受试者中,有四项受试者的血浆血管紧张素II浓度未能增加。尽管血浆肾素活性和血浆血管紧张素II浓度未改变或降低,但饮食钠限制后血浆醛固酮浓度仍显著增加。醛固酮产生的增加不能归因于血浆钠或钾浓度的变化或促肾上腺皮质激素分泌的增加。提示醛固酮对钠限制的反应不仅由血浆肾素活性和血管紧张素II浓度增加介导,还由另一种机制介导,可能与钠耗竭期间肾上腺对血管紧张素的敏感性增加有关。