Role of blood pressure in regulating Na+/H+ exchange in vascular smooth muscle

Na+/H+ exchange differs kinetically in mesenteric arteries from spontaneously hypertensive rats (SHR). Both the maximal transport rate and the sensitivity to [H+]i are greater in SHR than in Wistar Kyoto (WKY) rats. Kinetic changes are not seen in prehypertensive SHR or in SHR rendered normotensive by captopril therapy. Thus, blood pressure affects the properties of Na+/H+ exchange in SHR. To determine whether elevated pressure would have similar effects on the WKY transporter, WKY rats were rendered hypertensive by treatment with deoxycorticosterone acetate (DOCA). Mesenteric arteries from these animals were loaded with the pH-sensitive dye BCECF and Na+/H+ exchange activity was assessed by measuring the Nao-dependent, dimethyl amiloride-sensitive recovery of intracellular pH after acid loading. Treatment with DOCA/salt (two injections of 30 mg of DOCA/kg per week for 4 weeks + 1% NaCl in the drinking water) produced a significant increase in mean arterial pressure (181 +/- 29 v 108.1 +/- 6.2 in DOCA/salt v untreated controls), but had no effect on Na+/H+ exchange. Maximal transport rates for untreated, DOCA/salt-treated, and salt-treated rats were virtually identical (0.088 +/- 0.001, 0.103 +/- 0.011, and 0.093 +/- 0.006 mmol/L H+/sec, respectively. Moreover, the sensitivity of Na+/H+ exchange to internal H+ (ie, the Hill coefficient) was unchanged (n(app) = 4.3, 3.7, and 4.0, respectively). Because elevation in blood pressure produced no significant alterations in the WKY Na+/H+ exchanger, it seems likely that there are strain differences in the exchanger and/or in processes regulating its activity.