Angiotensin-dependent renal mechanisms in two-kidney, one-clip renal vascular hypertension.
Our understanding of the physiology of the renin-angiotensin system has advanced remarkably in the last decade as a result of the development of several pharmacologic agents that effectively block components of this humoral cascade. The use of these antagonists has also advanced our understanding of the contribution of the renin-angiotensin system to the development and maintenance of two-kidney, one-clip renal vascular hypertension. These antagonists have contributed greatly to the characterization of the systemic hemodynamic changes that occur in this model and, particularly, to the delineation of the behavior of the nonclipped kidney, a previously normal kidney that is subjected acutely to an environment of elevated systemic blood pressure and the input of a variety of other extrinsic influences. This kidney not only allows the blood pressure to increase and persist at elevated levels but appears to actively participate in the development and propagation of the hypertension. Although a variety of mechanisms impinge on the function of the nonclipped kidney in this model, the goal of this review is to analyze the behavior of this kidney and how its functional state is perturbed, primarily by the influence of angiotensin, which is believed to be delivered to it by the systemic circulation.
D000818:Animals; D001066:Appetite; D001794:Blood Pressure; D004195:Disease Models, Animal; D006977:Hypertension, Renal / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation; D012084:Renin-Angiotensin System; D012965:Sodium Chloride; D014556:Urine; D014655:Vascular Resistance
D012965:Sodium Chloride