Na+,K+-ATPase activity and responsiveness of vascular smooth muscle to norepinephrine, angiotensin II and calcium ionophore A23187 in guinea pig aortic strips.

The functional significance of the Na+,K+-ATPase activity in defining the sensitivity of vascular smooth muscle response to pressor stimuli was studied in guinea pig aortic strips. Subthreshold doses of ouabain (10(-8), 10(-7), 10(-6)M), potentiated the norepinephrine- and angiotensin II-induced contractile responses, dose-dependently. Furthermore, in the presence of subthreshold dose of ouabain (10(-6)M), tension developments were observed with subthreshold doses of norepinephrine and angiotensin II. The mechanism by which subthreshold dose of ouabain potentiated the norepinephrine-induced contractile response was revealed to involve the enhancement both of sensitivity and contractile activity. Ouabain (10(-6)M) potentiated the norepinephrine- and A23187-induced contractile responses, even in the presence of verapamil. These facts indicate that suppression of the vascular Na+,K+-ATPase activity could favor the development of hypertension through potentiating contractile responses to various stimuli and that the potentiation could be a reflection, at least partly, of the decrease in Ca2+-efflux.