Abstract
IN THE course of studies on experimental arteriosclerosis in the albino rat (1, 2 and 3), it was noted that inhibition of thyroid hormone production by propyl thiouracil (4) had a protective effect against the development of cardiovascular and smooth muscle necrosis as well as against secondary calcification following standard renal injury. The parathyroid hormone likewise was believed involved in the production of these lesions since marked enlargement of the parathyroid glands was one of the alterations encountered most consistently (5 and 6), and since secondary hyperparathyroidism resulting from renal impairment has long been known to cause vascular damage and metastatic calcification (7).
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