Decreased angiotensin II response but unaltered cardiovascular pressor response to infused norepinephrine after sodium restriction and converting enzyme inhibition.

Although studies indicate that converting enzyme inhibitors such as captopril influence beta-adrenergic physiology, the data on alpha-adrenergic physiology is inconsistent. This study therefore examined the effects of captopril (50 mg/day for 5 days) during sodium restriction on the pressor response and on angiotensin II and neuropeptide Y levels to infused norepinephrine (0.01 to 0.1 micrograms/kg/min) in 17 hypertensive and 27 normotensive subjects. Angiotensin II increased significantly in response to infused norepinephrine during placebo administration (p < 0.001) but not during captopril administration (p = 0.15). Neuropeptide Y levels decreased in response to captopril (p = 0.02). Despite these changes the pressor response to infused norepinephrine was unchanged with captopril. These data support the conclusion that the antihypertensive action of captopril is unrelated to alterations in norepinephrine-mediated alpha-adrenergic pressor regulation. The finding of a decrease in neuropeptide Y levels may have relevance to the therapeutic effects of captopril.