Studies on Experimental Hypertension

Abstract

These experiments indicate that, in dogs at least, ischemia localized to the kidneys is a sufficient condition for the production of persistently elevated systolic blood pressure. When the constriction of both main renal arteries is made only moderately severe in the beginning, the elevation of systolic blood pressure is unaccompanied by signs of materially decreased renal function. In this respect the hypertension in these animals resembles the hypertension which is associated with so called benign nephrosclerosis in man. Subsequent increase of the constriction of the main renal arteries does not materially damage renal function, probably because of adequate development of accessory circulation. More delicate methods for detecting a change may yet prove that some damage does occur. Almost complete constriction of both main renal arteries, from the beginning, results in great elevation of systolic blood pressure which is accompanied by severe disturbance of renal function and uremia. This resembles the type of hypertension which is associated with so called malignant nephrosclerosis, in the sense of Fahr (17). In several of the animals with persistent elevation of systolic blood pressure, anatomical changes were observed in the glomeruli, vessels and parenchyma of the kidneys which are most probably directly referable to the ischemia. It is hoped that these investigations will afford a means of studying the pathogenesis of hypertension that is associated with renal vascular disease.

Rodent models of heart failure: an updated review

“…Since 1934, when Goldblatt and his co-workers induced an elevation of blood pressure by partial constriction of the renal artery of the dog [81], many successful models of renal-induced experimental hypertension have been developed in rats. In general, the procedure includes twokidney Goldblatt hypertension (constriction of one renal artery while the contralateral kidney is left intact) and onekidney Goldblatt hypertension (one renal artery is constricted and the contralateral kidney is removed) [280].…”

Effects of Restoration of Blood Flow on the Development of Aortic Atherosclerosis in ApoE −/− Mice With Unilateral Renal Artery Stenosis

“…One potential explanation for the lack of benefit in these trials is that renal ischemia causes irreversible atherogenic changes and that restoration of renal blood flow has no effect on mitigating the damage to the vasculature 4. Biological plausibility of this hypothesis is provided by numerous studies showing that decreased renal perfusion is associated with RAS activation,5 and data from animal models showing that even short‐term elevation in angiotensin II (Ang‐II) levels can accelerate the development of atherosclerosis and lead to changes in the arterial wall that persist even after Ang‐II levels return to baseline 6, 7, 8, 9, 10, 11. In addition, RAS has been shown to result in elevated oxidative stress, sympathoadrenergic activation, and impaired vasoactive responses, both within the kidney and the systemic microcirculation 12, 13…”

Submitral atheromatous lesions in monkey and man

“…Fed an atherogenic diet (see below) and made renal hypertensive by subjecting them to bilateral renal artery clipping (a modified Goldblatt procedure) (Goldblatt et al, 1934) for 48-64 weeks. Group 3 (n = 10).…”