Renovascular Hypertension

Abstract

Abstract-Experimental 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 Ⅲ arterioles Ⅲ glomerular filtration rate Ⅲ rats, spontaneously hypertensive Ⅲ renal artery Ⅲ hypertrophy Ⅲ hypertension, renal M ore than 150 years ago, Richard Bright first linked the kidney to high blood pressure, but it was another 100 years before Goldblatt firmly established the potential of the kidney to cause hypertension. Goldblatt et al 1 produced the first reliable form of experimental hypertension with the remarkably simple intervention of narrowing the main renal artery to perturb renal hemodynamics. Since then, interest in the kidney in the development of essential hypertension has waxed and waned, with considerable debate on whether the kidney is the initiator, potentiator, and/or victim of essential hypertension. 2,3 Most investigators currently believe that the abnormalities and damage seen in the kidney in hypertension are entirely secondary. In particular, hypertrophy of the renal vessel walls is thought to be part of a response common to all systemic arterial vessels during sustained elevation of arterial pressure.The main argument in recent years for the importance of the kidney in hypertension has come from Hall et al, 4 Guyton, 5 and Cowley. 6 This work is widely accepted as showing the pivotal role of the arterial pressure/Na ϩ excretion rate relation in long-term blood pressure control. However, the mechanisms responsible for shifting this relation toward the right-that is, toward a prohypertensive situation in humans-remain unknown. In this article, we argue that primary changes in the structure of the preglomerular vessel walls may be one key mechanism responsible for a right shift of the pressure/Na ϩ excretion relation in hypertension. 4 -6 Using the simple situation of main renal artery stenosis as a background, we examined evidence for structurally based na...

Renal Structural Properties in Prehypertensive Dahl Salt-Sensitive Rats

“…[17][18][19][20][21][22][23] Thus, in the spontaneous form of hypertension, such as that seen in SHR, it is assumed that these structural changes would promote an increase in renal vascular resistance, especially in the preglomerular vasculature, and thereby serve to maintain normal glomerular pressure in the face of systemic hypertension. 24 The intrarenal hemodynamics characterized by these structural properties is consistent with the hemodynamics obtained in SHR in vivo. 3,25,26 Similarly, there are previous reports examining the renal vascular structural designs in salt-induced hypertensive models.…”

Decreased Renal Cytochrome P450 2C Enzymes and Impaired Vasodilation Are Associated With Angiotensin Salt-Sensitive Hypertension

“…23,24 Likewise, angiotensin II-infused hypertensive rats demonstrate a further elevation in blood pressure when fed a high-salt diet, or "salt sensitivity." 25,26 In the present study, the combination of a high-salt diet and angiotensin II infusion resulted in a greater increase in systolic blood pressure, which confirms salt sensitivity of angiotensin II-induced hypertension reported previously using radiotelemetry to measure arterial blood pressure.…”

Zalecenia Sekcji Pediatrycznej Polskiego Towarzystwa Nadciśnienia Tętniczego dotyczące postępowania diagnostycznego i terapeutycznego w nadciśnieniu tętniczym u dzieci i młodzieży

“…The main cause of renovascular hypertension in this age group is FMD, but in 20-40% of cases renovascular hypertension is a complication of other conditions (syndromic renovascular hypertension), including neurofibromatosis type 1 (> 15%) [65][66][67]. Renovascular hypertension may also be caused by a congenital or acquired (e.g., transplant renal artery stenosis) stenosis of the main renal artery or additional renal arteries and/or segmental branches [68][69].…”