Hydroosmotic response of collecting tubules to ADH or cAMP at reduced peritubular sodium.

Changes in cytosolic Ca2+ activity have been implicated in the hydroosmotic response to vasopressin (VP) in amphibian urinary bladder; the level of cytosolic free Ca2+ may be regulated, in part, by a process of Na-Ca exchange across the basolateral cell membrane. To assess whether similar mechanisms operate in the mammalian nephron, the effect of low peritubular [NA] on the hydraulic conductivity (Lp) of the isolated perfused rabbit collecting tubule (CT) exposed to either 20 microunits/ml VP or 5 X 10(-5) M 8-[p-chlorophenylthio]-cyclic 3',5'-adenosine monophosphate (ClPheS-cAMP) was studied. Low peritubular [Na] had no effect on the basal water permeability of the CT. After exposure to VP, CTs bathed in 145 mM Na Ringer solution developed an Lp of 324 +/- 27 X 10(-7) cm.s-1.atm-1, while tubules bathed in 4 mM Na and 141 mM tetramethylammonium Ringer solution achieved an Lp of only 112 +/- 13 X 10(-7) cm.s-1.atm-1 (P less than 0.001). Inhibition of the VP response was estimated to be half-maximal when peritubular Na was 120 mM. The hydroosmotic response to ClPheS-cAMP was diminished by 44% of the control values when CTs were bathed in a 4 mM Na medium; this inhibition was greatly attenuated when the peritubular Ca concentration was reduced to 0.05 mM. These results are consistent with the view that 1) a Na-Ca exchange process operates at the basolateral surface of the mammalian cortical collecting tubule cells, and 2) elevated cytosolic Ca ion activity inhibits the increase in water permeability elicited by VP or cAMP in this nephron segment.