Angiotensin-Dependent Hypertension — Potential Pitfalls in Definition

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Abstract
The relation of the activity of the renin-angiotensin system to the pathogenesis of hypertension remains controversial. In an attempt to resolve this controversy, interruption of the renin-angiotensin system by pharmacologic technics is finding increasing use. One class of pharmacologic agents, exemplified by saralasin (1-sar, 8-ala angiotensin II), has an affinity for the angiotensin receptor but only a limited ability to "fire" it, thereby antagonizing the action of angiotensin II.1 It is not surprising that most studies have documented that these compounds, specifically saralasin, are partial agonists since they are produced by a modification of the parent compound's structure.2 Thus, these . . .