(Hypertension. 2000;36:648.)
© 2000 American Heart Association, Inc.
Colin Johnston - A Celebration |
From the Department of Physiology, Monash University, Melbourne, Australia.
Correspondence to Prof W.P. Anderson, Department of Physiology, PO Box 13F, Monash University, Victoria 3800, Australia. E-mail warwick.anderson{at}med.monash.edu.au
AbstractExperimental narrowing of the main renal artery to produce hypertension increases the aorta-glomerular capillary pressure difference and vascular resistance. This article examines the hypothesis that hypertension also may be caused by structural changes that narrow intrarenal blood vessels, similarly increasing preglomerular vascular resistance and the aortic-glomerular capillary pressure gradient. There is evidence of both wall hypertrophy and lumen narrowing of the preglomerular arteries in spontaneously hypertensive rats, with increased preglomerular resistance and aortic-glomerular capillary pressure difference. We have also attempted to induce structural changes in renal-preglomerular vessels experimentally by infusing angiotensin II at low doses (0.5 to 4.5 ng/kg per minute) into the renal artery of Sprague-Dawley rats and greyhound dogs for up to 4 weeks. This angiotensin II infusion produced apparent dose-related effects on preglomerular vessel structure and hypertension. The possibility that hypertension may be induced by structural changes in preglomerular resistance vessel walls, by simulation of the hemodynamic effects of main renal artery stenosis, deserves further investigation.
Key Words: angiotensin II arterioles glomerular filtration rate rats, spontaneously hypertensive renal artery hypertrophy hypertension, renal
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