1. Hypertension was induced in male Sprague-Dawley rats by left unilateral nephrectomy and deoxycorticosterone acetate-salt administration. After 5 weeks, arterial systolic blood pressure was significantly elevated in these animals (191.5 ± 6.0 mmHg, mean ± sd, n = 17) compared with age-matched, unoperated control animals (134.0 ± 4.2 mmHg, n = 8, P < 0.001).
2. The membrane potential of femoral artery vascular smooth muscle measured in vitro was −55.1 ± 6.3 mV (mean ± sd, n = 154) for normotensive and −50.8 ± 5.7 mV (n = 82) for hypertensive animals. The difference in membrane potential was significant (P < 0.001).
3. The relationship between the log of the extracellular K+ concentration and membrane potential was nonlinear over the extracellular K+ concentration range 2.5–20 mmol/l, and showed a small positive shift with hypertension.
4. Tenfold reductions in the extracellular concentrations of Na+ or Cl− resulted in a membrane potential hyperpolarization in vascular smooth muscle from normotensive animals (4.9 ± 2.0 mV, n = 13 and 12.1 ± 1.3 mV, mean ± sd, n = 14, respectively). In vascular smooth muscle from hypertensive animals, the hyperpolarization in low-Na+ media was significantly increased to 12.2 ± 2.6 mV (mean ± sd, n = 5), but that in low-Cl− media was unaffected (2.7 ± 1.6 mV, n = 6).
5. The loop diuretic, bumetanide (10 μmol/l), hyperpolarized the membrane potential in vascular smooth muscle from both normotensive and hypertensive rats, but not in low-Na+ or low-Cl− media. This effect was significantly increased in hypertension, from 1.8 ± 0.7 mV (mean ± sd, n = 8) to 4.0 ± 1.0 mV (n = 5).
6. These results suggest that in these cells, K+ permeability ≫ Na+ permeability > Cl− permeabilty, and that the membrane potential is determined principally by the K+ permeability. In deoxycorticosterone acetate-salt hypertension, the membrane potential is depolarized, Na+ permeability is substantially increased, and there appears to be an increase in the activity of the (Na+-K+-Cl−) co-transporter.