LOW NA+ DIET INHIBITS NA+ AND WATER TRANSPORT RESPONSE TO VASOPRESSININ RAT CORTICAL COLLECTING DUCT

Background. We previously demonstrated that vasopressin (AVP) produces a sustained increase in Na+ reabsorption by the isolated perfused cor tical collecting duct (CCD) from rats on a normal diet, and that this effect is synergistic with that of pharmacological doses of deoxycorti costerone (DOC) or physiological levels of aldosterone. The present ex periments examined the effect of AVP under the more physiological circ umstances when plasma aldosterone was elevated by prior volume depleti on. Methods. Rats were volume depleted by a single dose of furosemide followed by a low-salt diet (0.3% NaCl) for four to nine days. Some of these rats were also implanted with a pellet containing 2.5 mg DOC. R ats in a third group were not injected with furosemide but were implan ted with the DOC pellet and maintained on a standard (similar to 1% Na Cl) diet. CCD were perfused and the lumen-to-bath Na+ flux (J(Na)), tr ansepithelial voltage (V-T), and osmotic water permeability (P-f) were measured in the presence and absence of 200 pM AVP. Results. Although Na+ depletion by a single injection of furosemide and the low salt di et elevated plasma aldosterone and V-T, J(Na) remained low and there w as a decreased response to AVP in comparison with DOC-treated rats on a standard diet. In CCD from rats on the low salt-diet with DOC, J(Na) was less than observed in CCD from DOC-treated rats on a standard die t. AVP-dependent P-f in CCD from rats on the low-salt diet, with or wi thout DOC treatment, was also markedly lower. Conclusions. We interpre t the results to demonstrate that maximal rates of Na+ reabsorption in the CCD depend not only on the synergistic stimulatory effects of ald osterone and AVP, but also require normal to high rates of salt delive ry in vivo for the effects of the hormones on Na+ transport to be maxi mized in vitro.