RAPID MODULATION OF RENAL AND ADRENAL RESPONSIVENESS TO ANGIOTENSIN-II

Reciprocal changes in adrenal and vascular responsiveness to angiotens in II (Ang II) are part of the normal adaptation to shifts in salt int ake. When dietary salt intake is abruptly reduced from high to low, en hancement in aldosterone secretion requires several days to develop. O nce established it is not known how quickly the enhancement is reverse d with salt repletion. We investigated the time course and relative co ntributions of salt, volume expansion, or both to this process by stud ying 15 normotensive subjects; 5 were studied during both high-salt an d low-salt balance, and 10 were studied only in low-salt balance. For rapid volume expansion to reverse low-salt balance, 5 subjects receive d in random order an infusion of normal saline or dextran. The adrenal glomerulosa and renal vascular responses to Ang II were assessed afte r each volume expansion maneuver. Saline and dextran infusions suppres sed plasma renin activity and aldosterone equally, although dextran ac ted more slowly. Both also increased renal perfusion and renal vascula r and presser responses to Ang II, which in 3 to 7 hours became identi cal to responses seen during high-salt intake (''modulation''). Saline infusion also blunted adrenal responsiveness to Ang II during that sa me interval. Despite suppression of the renin-angiotensin system by de xtran infusion, aldosterone responsiveness to Ang II remained enhanced . These observations suggest that the renal and vascular responses to Ang II are modulated rapidly by the effects of volume expansion per se . For the adrenal, modulation is also rapid, but a unique effect of sa line (sodium and/or chloride), independent of plasma volume expansion, is responsible for the swift change in aldosterone responsiveness to Ang II in salt-restricted normotensive subjects.