Production of occlusive vascular lesions by bacterial endotoxin in kidneys of rats with deoxycorticosterone hypertension.

Deoxycorticosterone acetate (DOCA) produces a characteristic syndrome in partially nephrectomized rats kept on a high sodium diet, which in many ways resembles the morphologic and functional aspects of human hypertensive vascular disease.' 2 The administration of renincontaining kidney extract to such rats, according to Masson, Corcoran and Page,3 results in an eclampsia-like syndrome with renal vascular lesions primarily involving the glomeruli. In the course of our study of DOCA hypertension in the rat, an attempt was made by various means to alter the course of the disease. This report describes the morphologic alterations noted after the administration of 5-hydroxytryptamine (5HT), bacterial endotoxins, and renin-containing kidney extracts (renin) to DOCA-hypertensive rats. The effects of renin previously observed8 are confirmed in this report. 5HT was given in view of its reported nephrotoxicity4 and its suggested role in the etiology of essential hypertension5 and eclampsia.8 Bacterial endotoxins are known to be vasculotoxic. Their administration in various species results in renal cortical necrosis and also intravascular deposition of fibrinoid,7 features which are at times encountered in different forms of hypertensive vascular disease. Our observations show some histologic similarities between the renal lesions caused by renin and endotoxin. Moreover, demonstrating that the renal vasculature in DOCA-hypertensive rats is unusually reactive to bacterial endotoxin, the present study may have implications in relation to the pathogenesis of human eclampsia and malignant nephrosclerosis.