SYNERGISTIC ACTION OF VASOPRESSIN AND ALDOSTERONE ON BASOLATERAL NA+-K+-ATPASE IN THE CORTICAL COLLECTING DUCT

The respective effects of aldosterone and arginine vasopressin (AVP) were examined on the number of active Na+-K+-ATPase and their pumping activity in nonperfused microdissected mouse cortical collecting tubules (CCD) by measuring specific H-3-ouabain binding and ouabain-sensitive Rb-86 uptake. In adrenalectomized (ADX) animals, incubation of CCD with AVP (10(-8) M for 5 min) had no effect on the number of pumps. In contrast, in ADX animals replete with aldosterone, AVP induced a congruent to 40% increase in the number of pumps. This was accompanied by a congruent to 60-65% increase in ouabain-sensitive Rb uptake. AVP effect was dose-dependent (10-(10)-10(-8) M) and was reproduced by dDAVP, forskolin and 8-Br cAMP, indicating a V-2 pathway. It was inhibited by amiloride 10(-5) M, and did not occur in CCD incubated in hyperosmotic solution, suggesting that the signal was transmitted via apical sodium entry and cell swelling. Finally, the AVP-dependent increase in the number of pumps was rapid (within 5 min) and transient (<25 min). These results demonstrate that, in the CCD, aldosterone and AVP act synergistically to increase not only the Na+-K+- apical sodium entry but also me basolateral Na+-K+-ATPase transport capacity: AVP allows a rapid recruitment and/or activation of an aldosterone-dependent pool of latent Na+-K+-ATPase.