Studies on the Pathogenesis of Hypertensive Vascular Disease

Abstract

Repeated high-pressure injection of saline into the arterial system via carotid cannula in normal, ether-anesthetized rats has been previously shown to produce acute necrotizing lesions in the renal vasculature. In this study administration of the vasodilator aminophylline prior to high-pressure injections led to similar lesions, produced in dilated, hyperdistended vessels, at far lower pressures than in control animals, demonstrating that neither vasoconstriction nor the absolute height of blood pressure is a critical determinant in production of lesions. In the second part of the study previous treatment with desoxycorticosterone (DOCA)-saline for 12 to 18 days rendered the renal vasculature abnormally prone to lesions after high-pressure injections, compared with normal rats so injected or those receiving a DOCA-saline regimen only. Glomerular lesions were more severe than can be explained on the basis of simple addition of the lesions resulting from high-pressure injections to those arising from DOCA administration. This increased susceptibility of the vasculature to elevated pressure is probably a function of focal alteration of vascular smooth muscle. These observations support the proposal that hypertensive vascular lesions occur in dilated, hyperdistended vessels and the glomeruli distal to them, the dilatation probably resulting from focal smooth muscle alteration with partial or complete loss of contractility.