1. Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. The hypothesis was tested that these changes in responsiveness of the zona glomerulosa are mediated in part by changes in plasma atrial natriuretic factor levels.
2. To this end, plasma renin activity and plasma aldosterone were measured in the upright and recumbent position and during incremental infusions of angiotensin II (1, 3 and 6 ng of angiotensin II amide min−1 kg−1 for 1 h each dose) after 6 days of sodium loading (study 1), after 5 days of sodium depletion (study 2) and after sodium depletion plus infusion of atrial natriuretic factor (0.13 μg/min for 8 h) on the test day (study 3). Six normal young males were investigated.
3. Plasma atrial natriuretic factor levels were around 5 pmol/l in study 2, 15 pmol/l in study 1 and 15 pmol/l in study 3 during infusion of atrial natriuretic factor. Two hours after the onset of atrial natriuretic factor infusion, plasma renin activity and plasma aldosterone (recumbent) were markedly and significantly lower in study 3 than in study 2, but still significantly higher than in study 1. The increase in plasma aldosterone after infusion of angiotensin II was slightly, but not significantly, blunted by infusion of atrial natriuretic factor in study 3 compared with study 2. The overall increase in plasma aldosterone was still significantly greater in study 3 than in study 1.
4. The fall in renal plasma flow, determined as p-aminohippurate clearance, during infusion of angiotensin II was greater in study 1 than in studies 2 and 3. Small differences between study 3 and study 2 were not significant.
5. It is concluded that infusions of atrial natriuretic factor in the low-sodium state that mimic plasma atrial natriuretic factor levels after sodium loading lead to a marked fall in recumbent plasma aldosterone, which is to a large extent secondary to a fall in plasma renin activity. A small direct effect of these physiologically elevated atrial natriuretic factor levels on the zona glomerulosa itself (the increase in plasma aldosterone during angiotensin II infusion) was only of borderline significance. Thus, atrial natriuretic factor at physiological plasma concentrations is a regulator of renin and aldosterone secretion, whereas a modulating effect on the renal vasoconstrictor action of angiotensin II could not be demonstrated.