Electrical property and chemical sensitivity of vascular smooth muscles in normotensive and spontaneously hypersensitive rats.

1. The membrane properties and sensitivity to chemical substances of smooth muscle cells of the portal vein and pulmonary artery were studied in normotensive rats (Wistar Kyoto) and spontaneously hypertensive rats (Okamoto & Aoki) by the micro-electrode method. 2. The parameters of the membrane, i.e. resting membrane potential, the maximum rate of rise of the spike, space constant of the tissue and time constant of the membrane measured from the portal vein were the same in normotensive rats (less than 120 mmHg) and spontaneously hypertensive rats (greater than 165 mmHg). Similar results were also obtained from the pulmonary artery. Such findings indicate that the passive electrical properties of the vascular muscle membrane are not involved in the generation mechanism of hypertension. 3. In the portal vein the maximum slope of the membrane depolarization produced by tenfold increase in external K+ concentration expressed on a logarithmic scale was the same in normal and hypertensive rats (42 and 41 mV, respectively). These observations were confirmed by the effects of application of excess K+ on the pulmonary artery (48 mV in normal and 46 mV in hypertension). With a low concentration of K+, the membrane was depolarized to a greater extent in the portal veins than in the pulmonary arteries of both types of rats. Although the response to K+ differed in vascular muscles excised from the different regions, no functional difference was apparent between normotensive and hypertensive. 4. In both portal vein and pulmonary artery, the smooth muscle membrane of spontaneously hypertensive rats proved to be more sensitive to noradrenaline, i.e. depolarization of the membrane appeared with noradrenaline 10(-9) g/ml. in hypertensive but with 10(-8)g/ml. in normotensive rats. Depolarization block of the spike generation appeared at a slower concentration of noradrenaline in hypertensive rats. Sensitivity of the smooth muscle membrane to prostaglandin E2 in the portal vein was also higher in hypertensive rats. 5. The present results indicate that the only difference between normal and spontaneously hypertensive rats regarding smooth muscle cell membrane of the pulmonary artery and portal vein is increased chemical sensitivity in hypertensive rats, and the passive electrical properties of the membrane probably does not contribute to the generation of hypertension.