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

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Abstract
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.alpha.-fludrocortisone acetate (9.alpha.F; 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 9.alpha.F 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 9.alpha.F 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 9.alpha.F-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 9.alpha.F (P < 0.05) but not during prednisone administration. Plasma renin, aldosterone, and norepinephrine (NE) decreased during 9.alpha.F 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 9.alpha.F but not prednisone administration, while blood pressure reactivity to NE was not significantly modified. These findings demonstrate that 9.alpha.F 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.