HYPERTENSIVE VASCULAR LESIONS OF TESTICULAR ARTERIES ASSOCIATED WITH ALTERATION OF FIBROUS PROTEIN OF TESTES IN STROKE-PRONE AND -RESISTANT SPONTANEOUSLY HYPERTENSIVE RATS

Abstract

Stroke-prone and -resistant spontaneously hypertensive rats were treated with pepstatin or clonidine from 6 weeks of age to 8 weeks of age. Fiborus protein of testes or in vivo incorpotation of ³H-lysine into the protein fractions was determined in each rat strain on the final day.
Significant differences were noted between hypertensive rats and normotensive Wistar Kyoto rats, the former rats having greater incorporation rates of ³H-lysine into non-collagenous protein in testicular or mesenteric artery than the normotensive rats. Administration of clonidine decreased the incorporation of ³H-lysine into non-collagenous protein or collagen in the testicular artery concomitantly with the reduction of blood pressure in each rat strain. Pepstatin failed to reduce the incorporation of ³H-lysine into these protein fractions in any vessels examined, and it also failed to alter the blood pressure in hypertensive rats. The amonut of collagen or elastin in testes of hypertensive rats was greater than that of normotensive rats. The data indicate that increased non-collagenous protein and collagen in testicular arteries or mesenteric arteries in SHR or SHRSP can raise the blood pressure in its early hypertensive stage. In addition, increased amount of collagen and elastin in testes of SHRSP apperars tobe derived from hypertensive lesions of testicular arteries.