The long-term inhibitory effect of ANF on aldosterone secretion is mediated by both renin release blockade and direct action on the zona glomerulosa.
Animal data support dual renin-dependent and direct aldosterone suppression by ANF; human relevance remains untested.
Prolonged (12-day) sodium deprivation strikingly raised both basal plasma aldosterone concentration (PAC) (114%) and plasma renin activity (PRA) (200%), and lowered ANF blood level (-30%). Acute ANF bolus administration produced a dose-dependent decrease in PAC in both normally-fed and sodium-restricted rats. The maximum effect (-30/-37%) was observed with a dose of 20 micrograms.kg-1. The interruption of the renin-angiotensin system (RAS), obtained by a 7-day infusion of captopril and maintenance doses of angiotensin II, did not cause significant changes in PAC in animals kept on a normal diet, while it did induce a significant lowering of PAC in sodium-restricted rats (-25%). This treatment evoked in both groups of animals a notable reduction of PRA (-61/-89%). A 7-day infusion with ANF (at a rate of 20 micrograms.kg-1.h-1) notably lowered PAC (-32%) in normally-fed rats, independently of the RAS status. The same occurred in sodium-deprived rats, but the effect was more intense in animals with intact RAS (-41% vs -24%). Prolonged ANF infusion significantly reduced PRA (-48%) only in sodium-restricted rats with intact RAS. These findings suggest that (i) the long-term inhibitory effect of ANF on aldosterone secretion is due to both the block of renin release and a direct action on the zona glomerulosa; and (ii) the mechanism underlying the adrenoglomerulotrophic effect of sodium restriction involves not only the activation of RAS, but also the suppression of ANF release.
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Nussdorfer et al. (1988) studied this question.
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