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Glucocorticoid and Mineralocorticoid Stimulation of Atrial Natriuretic Peptide Release in Man^*

Medizinische Poliklinik, University of Bern 3010 Bern, Switzerland

Address all correspondence and requests for reprints to: Peter Weidmann, M.D., Medizinische Universitäts Poliklinik, Freiburgstrasse 3, 3010 Bern, Switzerland.

To investigate the influence of a mineralocorticoid and a glucocorticoid on plasma immunoreactive atrial natriuretic peptide (irANP) and possible functional correlates, eight normal men received in random order 9-fludrocortisone acetate (9F; 0.6 mg/day), prednisone (50 mg/day), and placebo each for 9 days. Their diet contained 130 mmol sodium and 75 mmol potassium daily. The mean supine plasma irANP levels were similar on days 2, 4, and 9 of placebo treatment [25 ± 10 (±SE), 27 ± 5, and 27 ± 6 pmol/L, respectively]. Mean plasma irANP levels were 76 ± 42 (P < 0.05), 89 ± 34, and 93 ± 29 pmol/L (P < 0.01), respectively, on days 2, 4, and 9 during 9F administration, and 68 ± 37 (P < 0.05), 83 ± 41, and 48 ± 18 pmol/L on the same days during prednisone administration. Compared with the placebo period, sodium intake minus urinary output during 9F administration averaged +41 mmol at the time of blood sampling on day 2, +112 mmol on day 4, and +149 mmol on day 9; body weight was unchanged on day 2 and increased by 0.7 and 1.1 kg on days 4 and 9, respectively. Escape from 9F-induced renal sodium retention occurred on days 5 and 6. During prednisone administration, sodium intake minus urinary output and body weight did not change. Plasma volume and BP rose significantly during 9F (P < 0.05) but not during prednisone administration. Plasma renin, aldosterone, and norepinephrine (NE) decreased during 9F treatment (P < 0.05 to < 0.01); during prednisone treatment, plasma aldosterone levels were lower on day 9 only. Cardiovascular pressor responsiveness to angiotensin II was enhanced during 9F but not prednisone administration, while blood pressure reactivity to NE was not significantly modified. These findings demonstrate that 9F and prednisone in high doses provoke remarkably similar increases in plasma irANP, but that the glucocorticoid-induced rise in plasma irANP is due to a mechanism other than sodium and volume retention.

^* This work was supported in part by the Swiss National Science Foundation and a Research Grant from the Ciba Geigy Corp. (Basel, Switzerland).

Received September 21, 1987.