Activation of two inward chloride transport systems in rat femoral arterial smooth muscle in deoxycorticosterone acetate/salt hypertension.

1. Intracellular [Cl-] ([Cl-]i) was measured with ion-selective microelectrodes in rat femoral arterial smooth muscle in normotensive controls and after the induction of deoxycorticosterone acetate/salt hypertension. 2. Linear regression of [Cl-]i and time after the induction of hypertension showed good correlation (r = 0.96) for 5-6 weeks, as [Cl-]i increased from 30 +/- 1 mmol/l (mean +/- SD, n = 16), to 49 +/- 2 mmol/l (n = 9, P < 0.0001). 3. Arterial systolic blood pressure also increased linearly (r = 0.97) for 5-6 weeks as hypertension developed from 122 +/- 1 mmHg (n = 20) to 187 +/- 7 mmHg (n = 14): there was consequently a linear relationship between [Cl-]i and arterial systolic blood pressure (r = 0.96). 4. The increase in [Cl-]i was partly because Na(+)-K(+)-Cl- co-transport activity, estimated from the fall in [Cl-]i caused by bumetanide, was greater in hypertension (18 mmol/l) than in normotension (10 mmol/l). This finding, and the depolarization of the membrane potential in hypertension (-56 +/- 3 mV compared with -64 +/- 4 mV in normotension; P < 0.0001), confirms previous studies. 5. The increase in [Cl-]i was also partly due to greater activity of an Na(+)- and HCO3(-)-independent, acetazolamide-sensitive inward Cl- transport system; thus acetazolamide reduced [Cl-]i by 7 mmol/l in normotension and by 16 mmol/l in hypertension. 6. In Cl(-)-free media, the membrane potential in normotension (-59 +/- 5 mV) was not significantly different from that in hypertension (-60 +/- 4 mV). 7. The role of [Cl-]i in the depolarization of the membrane potential in hypertension is discussed.