Jungmann E, Ackerman A, Panijel-Rath C, Schöffling K
Med Klin Prax. 1982 Apr 9;77(8):58-63.
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.
直到六十年代后期,血管紧张素一直被视为醛固酮分泌的主要刺激因素,当时有关醛固酮释放调节的讨论再度兴起。本研究展示了八名健康志愿者的血浆肾素活性、血清醛固酮以及血清和尿液中的电解质对促肾上腺皮质激素(静脉注射0.25毫克合成促肾上腺皮质激素)、地塞米松预处理(口服2毫克米力可松)以及速尿(静脉注射40毫克速尿)+钾(口服80毫摩尔卡利诺)和速尿+普萘洛尔(静脉注射5毫克多喜通)联合给药的反应。血浆肾素活性和醛固酮通过放射免疫测定法测量,血清和尿液中的电解质按照常规方法测定。促肾上腺皮质激素增加醛固酮但不影响血浆肾素活性。地塞米松预处理降低醛固酮并刺激肾素对直立姿势的反应。钾延迟速尿后血浆肾素活性的增加,普萘洛尔抑制速尿诱导的肾素释放,两者均不损害醛固酮分泌。我们得出结论,醛固酮产生的调节系统远比肾素-血管紧张素-醛固酮系统概念所表明的更为复杂。