A reduced sensitivity to the pressor effect of exogenous angiotensin 1 has been observed in dogs with increased levels of endogenous angiotensinlike activity (1). Patients with secondary hyperaldosteronism, where levels of endogenous angiotensin are thought to be elevated, also have a reduced pressor responsiveness to exogenous angiotensin, but not to l-norepinephrine (2, 3). A reduced pressor responsiveness to angiotensin might then be expected with renovascular hypertension, which is said to be associated with increased levels of circulating renin and angiotensin (4). The pressor responses to exogenous angiotensin and, in some patients, to l-norepinephrine were initially examined in a variety of experimental and pathological situations where the levels of endogenous angiotensin have either been shown or are believed to be altered. Patients with various hypertensive diseases were then studied. The results suggest that the pressor responsiveness to angiotensin may be a useful clinical test for the diagnosis of renovascular hypertension.
Kaplan et al. (Wed,) studied this question.