In the isolated aorta, the increase in tension provoked by addition of KC1 16.7mM was attenuated by enalapril treatment(3mg/kg/day for 6 weeks), whereas the increment by addition of NE 0.1uM tension was not influenced. The frequency-dependent vasoconstricution induced by electrical field stimulation of aorta was also attenuated by enalapril treatment. In pithed SHR, the frequency-related hypertension provoked by electrical stimulation(10sec, 1ms with 40V) of sympathetic pregnglionic nerve was also attenuated by enalapril treatment. Neither dose-related vasorelaxation by acetylcholine addition in the aorta nor decrease of DBP by intravenously(i.v.)-injected aetylcholine was altered by enalapril treatment. However, β2-agonist, salbutamol-induced vasorelaxation in enalapril-treated group, was more remarkable than that in control group. The hypotension by i.v.-but not by intracerebroventricularly-injected salbutamol strengthened by enalapril treatment.

These results suggest that the suppression of development of hypertension by enalapril treatment may result from the reduction of adrenergic neurotransmission and activity to voltage dependent calcium channel by acting on vascular smooth muscle itself.