Unraveling the Mystery of Goldblatt Hypertension

Author:

Navar L. Gabriel1,Zou Lixian1,Von Thun Annette1,Tarng Wang Chi1,Imig John D.1,Mitchell Kenneth D.1

Affiliation:

1. L. G. Navar, J. D. Imig, and K. D. Mitchell are in the Dept. of Physiology, Tulane University School of Medicine, New Orleans, LA 70112, USA; L. Zou was a Postdoctoral Fellow in that Department. A. Von Thun is in the Dept. of Internal Medicine of the Naval Medical Center, San Diego, CA, USA. C. T. Wang is in the Dept. of Internal Medicine, Section of Nephrology, General Hospital, Taipei, Taiwan.

Abstract

In hypertension caused by unilateral renal artery stenosis, the nonstenotic kidney becomes renin depleted but fails to prevent hypertension. The nonstenotic kidney mysteriously develops elevated intrarenal angiotensin II (ANG II) content. Rats chronically infused with ANG II exhibit a similar hypertensive process. The augmentation of intrarenal ANG II is due to receptor-mediated internalization and continued ANG II formation, which provide a hypertensinogenic stimulus.

Publisher

American Physiological Society

Subject

Physiology

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