Pathogenesis of Experimental Arteriosclerosis in the Rat.

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Abstract
The pathogenesis of severe arteriosclerosis and disseminated myocardial necrosis, induced in the albino rat by standard renal injury, was studied. These cardiovascular lesions are due to autointoxication with parathyroid hormone, and this hormone apparently contains an important hypertensive factor. Excess production of parathyroid hormone as a consequence of renal dysfunctions is mediated through the adrenal cortex and mineralocorticoids are essential for the direct or indirect activation of the parathyroid gland. To some degree, androgens can enhance the mineralocorticoid effect, whereas estrogens seem to inhibit the emergence of muscular necrosis. The incidence of cardiovascular injury in intact and adrenalectomized rats was sub-sstantially higher in male than in female animals. In the absence of the parathyroid glands, mineralocorticoids in excessive dosage fail to produce cardiovascular necrosis, whereas excess parathyroid hormone assures the emergence of typical lesions in the complete absence of mineralocorticoids. In fact, by providing abundant supplies of parathyroid extract, cardiovascular necrosis was induced without renal injury and even in the absence of the kidneys. The implications of these findings upon the concept of "metastatic calcification" and upon the pathogenesis and therapy of renogenic cardiovascular necrosis and hypertension in human beings are discussed. It is suggested that subtotal parathyroidectomy be tried in preference to adrenalectomy in attempts to arrest the rapidly progressive sequelae of malignant hypertension.

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