[Various aspects of the regulation of aldosterone secretion].

Medizinische Klinik (Praxis-Ausg.) Pub Date : 1982-04-09
E Jungmann, A Ackerman, C Panijel-Rath, K Schöffling
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Abstract

Angiotensin was regarded as the major stimulus of aldosterone secretion until the late sixties, when the discussion about the regulation of aldosterone release has been renewed. The present study demonstrates the response of plasma renin activity, aldosterone in serum and electrolytes in serum and urine to ACTH (0.25 mg Synacthen i.v.), pretreatment with dexamethasone (2 mg Millicorten p.o.) and to combined administrations of furosemide (40 mg Lasix i.v.) + potassium (80 mmol Kalinor p.o.) and furosemide + propranolol (5 mg Dociton i.v.) in eight healthy volunteers. Plasma renin activity and aldosterone were measured by radioimmunoassay, electrolytes in serum and urine according to routine methods. ACTH increases aldosterone without influencing plasma renin activity. Pretreatment with dexamethasone decreases aldosterone and stimulates renin response to upright posture. Potassium delays the increase of plasma renin activity after furosemide and propranolol inhibits the furosemide-induced renin release, both without impairing aldosterone secretion. We conclude that the regulatory system of aldosterone production is far more complex than suggested by the concept of the renin-angiotensin-aldosterone-system.

【醛固酮分泌调节的各个方面】。
血管紧张素一直被认为是醛固酮分泌的主要刺激物,直到60年代末,关于醛固酮释放调控的讨论才重新开始。本研究显示血浆肾素活性、血清醛固酮、血清和尿液电解质对ACTH (0.25 mg Synacthen静脉注射)、地塞米松预处理(2 mg Millicorten静脉注射)、呋塞米(40 mg Lasix静脉注射)+钾(80 mmol Kalinor静脉注射)和呋塞米+普萘洛尔(5 mg Dociton静脉注射)的反应。用放射免疫法测定血浆肾素和醛固酮活性,按常规方法测定血清和尿液电解质。ACTH增加醛固酮而不影响血浆肾素活性。地塞米松预处理降低醛固酮,刺激肾素对直立姿势的反应。钾延缓了呋塞米后血浆肾素活性的增加,而心得安则抑制了呋塞米诱导的肾素释放,两者均不影响醛固酮的分泌。我们得出结论,醛固酮生产的调控系统远比肾素-血管紧张素-醛固酮系统的概念所暗示的要复杂得多。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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