Kraiem Z, Rosenthal T, Rotzak R, Lunenfeld B
Acta Endocrinol (Copenh). 1979 Aug;91(4):657-65. doi: 10.1530/acta.0.0910657.
Twelve healthy male volunteers on a normal Na and K intake and ambulatory received ACTH (40 IU, im) twice daily for 5 days followed by 2 days of angiotensin II (5--13 ng/kg body weight/min for 60 min) or oral K citrate (30 mEq./h x 3). A discordance in the aldosterone-stimulating and pressor responses of angiotensin II was unmasked with only the latter response being positive following ACTH-induced refractoriness. K loading was a much more potent natriuretic stimulus than angiotensin II treatment. In contrast to angiotensin II, K could selectively enhance aldosterone secretion by overcoming the inhibition in secretion of the mineralocorticoid induced by prolonged ACTH exposure.
12名健康男性志愿者，钠和钾摄入正常且可自由活动，每天接受两次促肾上腺皮质激素（40国际单位，肌肉注射），共5天，随后2天接受血管紧张素II（5 - 13纳克/千克体重/分钟，持续60分钟）或口服柠檬酸钾（30毫当量/小时×3）。在促肾上腺皮质激素诱导的不应期后，血管紧张素II的醛固酮刺激反应和升压反应出现不一致，仅后者反应为阳性。钾负荷是比血管紧张素II治疗更强的利钠刺激因素。与血管紧张素II不同，钾可以通过克服长期促肾上腺皮质激素暴露诱导的盐皮质激素分泌抑制来选择性增强醛固酮分泌。
