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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-) co-transport

Journal Article


Abstract


  • 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 ��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.

UOW Authors


  •   Harper, Alexander (external author)

Publication Date


  • 1991

Citation


  • Davis, J. P. L., Chipperfield, A. R., & Harper, A. A. (1991). 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-) co-transport. Clinical Science, 81(1), 73-78. doi:10.1042/cs0810073

Scopus Eid


  • 2-s2.0-0025765275

Start Page


  • 73

End Page


  • 78

Volume


  • 81

Issue


  • 1

Place Of Publication


Abstract


  • 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 ��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.

UOW Authors


  •   Harper, Alexander (external author)

Publication Date


  • 1991

Citation


  • Davis, J. P. L., Chipperfield, A. R., & Harper, A. A. (1991). 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-) co-transport. Clinical Science, 81(1), 73-78. doi:10.1042/cs0810073

Scopus Eid


  • 2-s2.0-0025765275

Start Page


  • 73

End Page


  • 78

Volume


  • 81

Issue


  • 1

Place Of Publication