Glucocorticoid and mineralocorticoid stimulation of atrial natriuretic peptide release in man.
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 less than 0.05), 89 +/- 34, and 93 +/- 29 pmol/L (P less than 0.01), respectively, on days 2, 4, and 9 during 9 alpha F administration, and 68 +/- 37 (P less than 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 less than 0.05) but not during prednisone administration. Plasma renin, aldosterone, and norepinephrine (NE) decreased during 9 alpha F treatment (P less than 0.05 to less than 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.
Weidmann
P
P
Medizinische Poliklinik, University of Bern, Switzerland.
Matter
D R
DR
Matter
E E
EE
Gnädinger
M P
MP
Uehlinger
D E
DE
Shaw
S
S
Hess
C
C
D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D001826:Body Fluids / Q000378:metabolism; D004573:Electrolytes / Q000378:metabolism; D004702:Endocrine Glands / Q000378:metabolism; D005438:Fludrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008901:Mineralocorticoids / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D011241:Prednisone / Q000494:pharmacology; D013268:Stimulation, Chemical
D004573:Electrolytes; D005938:Glucocorticoids; D008901:Mineralocorticoids; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D005438:Fludrocortisone; C034635:fludrocortisone acetate; D011241:Prednisone; D009638:Norepinephrine