This review summarizes the pathophysiology of renovascular hypertension based on the Goldblatt model, emphasizing the renin-angiotensin system and renal nerves.
Supports mechanistic focus on RAS and renal nerves in renovascular hypertension; leaves open targeted therapies pending prospective validation.
Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed.
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M. Martinez-Maldonado (1991) studied this question.
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