Glucocorticoid Hypersecretion and Hypertensive Vascular Disease in Experimental Malignant Hypertension in Rats

Abstract

1. Changes in plasma glucocorticoid levels and the alterations they imposed upon the lymphoid system and vascular hypertrophy were studied in rats developing either the benign or malignant forms of hypertension during the initial 30 days after aortic ligation. 2. A threefold increase in plasma corticosterone was observed during both the acute and chronic phases of malignant hypertension, whereas in benign hypertension, after a short-lasting twofold increase, corticosterone returned to normal within 9 days. 3. Thymus atrophy, thymocyte depletion and impaired thymocyte reactivity characterized the acute phase of benign and malignant hypertension. After 9 days these alterations receded in benign hypertension, whereas they were permanent features accompanied by severe lymphocytopenia and marked neutrophilia in malignant hypertension. 4. Syntheses and contents of collagen and elastin were impaired in the arteries of malignant hypertensive rats. In contrast, elevated synthesis and increased deposition of these proteins were observed in benign hypertensive rats. Both forms of the disease were characterized by increased deposition of arterial non-fibrous protein. 5. Although acute arterial fibrinoid deposition was observed in benign and malignant hypertension, fibrinoid disappeared in benign hypertensive rats whereas it evolved into necrotizing lesions characterized by disruption of the arterial structure and lymphoid cell infiltration in malignant hypertensive rats. 6. These studies indicate that differing patterns of altered glucocorticoid secretion accompany the development of benign and malignant hypertension. These hormones, by altering the lymphoid system and arterial connective tissue metabolism may participate in the development and perpetuation of the necrotizing arterial lesions observed in malignant hypertension.