COMPARISON OF THE ELECTRICAL-PROPERTIES OF ARTERIAL SMOOTH-MUSCLE IN NORMOTENSIVE RATS AND RATS WITH DEOXYCORTICOSTERONE ACETATE SALT-INDUCED HYPERTENSION - POSSIBLE INVOLVEMENT OF (NA+ -K+ -CL-) COTRANSPORT

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 non-linear 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-mu-mol/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- permeability, 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.