An analysis is presented of volume and vasoconstrictor factors in experimental renovascular hypertension. Volume expansion and increased cardiac output produced by renal retention of salt and water are not essential for chronic renovascular hypertension to develop. When volume expansion and increased cardiac output do occur, however, it appears that the increased cardiac output contributes directly to the hypertensive process without triggering myogenic alterations in peripheral resistance predicted by the whole-body autoregulation theory of hypertension. Activation of the renin-angiotensin vasoconstrictor mechanism is not essential for either the development or the maintenance of chronic one-kidney renovascular hypertension in either the dog or the rat. In experimental two-kidney renovascular hypertension, a clear species difference is apparent. In the two-kidney hypertensive dog, the angiotensin pressor mechanism appears to play only a transient role lasting about 1 wk. In the two-kidney Goldblatt hypertensive rat, however, both the development and the maintenance of the hypertension are angiotensin-dependent, at least for a 4- to 6-wk period. When both the volume component and the renin-angiotensin vasoconstrictor component were deleted in one-kidney rats by sodium depletion and chronic SQ 14225 administration, renal artery stenosis failed to produce chronic renovascular hypertension. It is concluded that the pathogenesis of chronic renovascular hypertension requires either volume expansion produced by renal salt and fluid retention or expression of the renin-angiotensin vasoconstrictor mechanism.