E Jungmann, A Ackerman, C Panijel-Rath, K Schöffling
{"title":"[Various aspects of the regulation of aldosterone secretion].","authors":"E Jungmann, A Ackerman, C Panijel-Rath, K Schöffling","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":79233,"journal":{"name":"Medizinische Klinik (Praxis-Ausg.)","volume":"77 8","pages":"58-63"},"PeriodicalIF":0.0000,"publicationDate":"1982-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medizinische Klinik (Praxis-Ausg.)","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.