Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension.

Parathyroidectomy (Px) did not prevent the development of deoxycorticosterone (DOC)-induced hypertension inasmuch as the systolic blood pressure at 4 weeks did not differ from that of parathyroid intact, DOC-treated rats. Px, however, ameliorated the percent incidence and severity index of hypertension-induced vascular lesions in the heart and kidney. There was less hyaline change in the coronary artery and renal arteriole and fewer scars in the myocardium of Px + DOC rats than in DOC-treated animals. Arterial hypertrophy in aorta, coronary artery, renal interlobular artery, and renal arteriole in hypertensive animals was not affected by Px. The aortic content of total calcium in the Px-hypertensive rats was reduced significantly as compared to parathyroid-intact hypertensive rats. The abdominal aorta in the Px + DOC group showed a greater reduction in calcium than the thoracic aorta. We conclude that calcium may not be essential in mediating hypertension-induced vascular hypertrophy. Parathyroidectomy permitted a separation of high blood pressure-hypertrophy from hyaline vascular lesions in DOC-induced hypertensive rats, likely acting upon endothelial cells to prevent movement of plasma proteins (hyaline change) from the vascular lumen into the media-subendothelial space of blood vessels.