Chronic small increases in circulating ANF can selectively blunt adrenocortical responses to aldosterone secretagogues without affecting pressor responses to angiotensin II.
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Hypothesis-generating in rabbits; leaves open whether chronic ANF modulates human renin-angiotensin-aldosterone responses.
This study assessed the effect of chronic infusions of atrial natriuretic factor (ANF) on in vivo and in vitro production of aldosterone. Vehicle (saline) or rat ANF-(99-126) was intravenously infused at 100 ng.kg-1.h-1 for 5 consecutive days into male New Zealand White rabbits. At 5 days plasma ANF was 18 +/- 4.1 pg/ml in vehicle-infused and 48.5 +/- 9.0 in ANF-infused rabbits (P less than 0.01). Plasma renin activity was significantly less in ANF-infused rabbits (2.99 +/- 0.35 vs. 0.77 +/- 0.12 ng.ml-1.h-1, P less than 0.01); however no differences were observed in the basal plasma concentrations of aldosterone, corticosterone, potassium, or hematocrit. In in vivo studies, chronically administered ANF attenuated plasma aldosterone, but not pressor, responses to acutely infused angiotensin II given at doses of 4, 16, and 64 ng.kg-1.min-1 for 20 min each. In in vitro experiments, collagenase-dispersed adrenal capsular cells from ANF-infused rabbits exhibited significantly reduced maximal responses to adrenocorticotropic hormone, angiotensin II, and potassium. These results suggest that chronic small increases in circulating ANF can blunt selectively adrenocortical responses to aldosterone secretagogues without affecting pressor responses to angiotensin II.
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Nagano et al. (1990) studied this question.
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