Specificity of altered electrogenesis of membrane potential in hypertension.

Cardiac and hepatic portal venous muscle were used in an attempt to determine the specificity of the altered membrane potential (Em) electrogenesis found in caudal artery of spontaneously hypertensive rats (SHR). Neither the sensitivity to norepinephrine nor the electrogenesis of Em was found to be different in SHR than in their normotensive controls. Thus, ventricular myocardium and portal venous myovascular cells do not show either the increased sensitivity or the Em factor proposed as a contributor to it. A second determination of specificity was stimulation of the caudal artery by Ba2+. Both depolarization and extent of contraction were no different in SHR than in normotensive controls, suggesting that the increased sensitivity of arterial muscle does not extend to all depolarizing agents. These data define the electrogenesis of Em in cardiac and portal venous muscle of SHR and their controls and provide a test of the hypothesis that altered Em electrogenesis contributes to increased arterial norepinephrine sensitivity seen in hypertension. The data support rather than refute the hypothesis, i.e., the Em alteration was specific for both the muscle showing increased sensitivity and the agent used for depolarization.