Lower Na(+)-H+ antiport activity in vascular smooth muscle cells of Wistar-Kyoto rats than spontaneously hypertensive and Wistar rats.

To determine whether increased Na(+)-H+ antiport activity in vascular smooth muscle cells may relate to the pathogenesis of hypertension in the spontaneously hypertensive rat (SHR), we monitored Na(+)-dependent alkalinization of acidified cells from the hypertensive strain and two normotensive controls, the Wistar-Kyoto rat (WKY) and the Wistar rat. Changes in intracellular pH (pHi) of cultured aortic cells were measured using the fluorescent probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The initial maximal reaction velocity of Na(+)-dependent alkalinization was significantly higher in SHR and Wistar than WKY cells. Similar results were obtained for the maximal velocity of the proton equivalent efflux: SHR, 7.51 +/- 0.71; Wistar, 9.14 +/- 0.85; WKY, 4.38 +/- 0.55 mmol H+/liter x 10 s. There were no differences in the basal pHi or cellular buffering power among the three rat strains. These findings indicate that the activity of the Na(+)-H+ antiport is higher in SHR vascular smooth muscle cells than in WKY cells. However, by itself, this difference cannot explain the hypertensive process in the SHR, since this transport system is also higher in vascular cells of the Wistar rat.