Enhancement of intracellular sodium by vasopressin in spontaneously hypertensive rats.

The arginine vasopressin-induced increase in intracellular sodium concentration was augmented in cultured rat vascular smooth muscle cells derived from 12-week-old spontaneously hypertensive rats (SHR) compared with those from 12-week-old normotensive Wistar-Kyoto (WKY) rats. This difference was enhanced by treatment with a Na+,K(+)-ATPase inhibitor, ouabain. The calcium-free state did not affect the basal intracellular sodium concentration but completely blocked the arginine vasopressin-induced increase in intracellular sodium concentration in both cell groups. The arginine vasopressin-mobilized cytosolic free calcium was enhanced in SHR compared with WKY rats. This enhancement was diminished but not completely inhibited in the calcium-free state. Also, arginine vasopressin-produced intracellular alkalinization was augmented in SHR. Pretreatment of both cell groups with a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, completely blocked arginine vasopressin-induced intracellular alkalinization and increased intracellular sodium concentration. Scatchard analysis showed that the V1 receptor number of either quiescent or proliferative cells of SHR was five to seven times greater than that of WKY rats, without any change in receptor affinity. These findings therefore indicate that the arginine vasopressin-induced increase in intracellular sodium concentration is augmented in vascular smooth muscle cells of SHR mediated through the enhancement of the mobilization of cytosolic free calcium and the activity of sodium-hydrogen exchange, which depends on an increase in V1 receptor number.