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.

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