Role of Arginine-Vasopressin (AVP) in Stress-Induced Inhibition of Testicular Steroidogenesis in Normal and in AVP-Deficient Rats*

It has been recently demonstrated that immobilization stress induces in rats a state of testicular desensitization to gonadotropins as well as a post-cAMP blockade of testosterone (T) biosynthesis. Since arginine-vasopressin (AVP) has recently been found to antagonize in rats the in vitro T-releasing effect of human CG, with this work we have verified whether AVP might be involved in stress-induced inhibition of T biosynthesis. In Sprague-Dawley and Long-Evans adult male rats chronically cannulated in the jugular vein, a small but statistically significant rise of plasma AVP levels was observed after 2 h of immobilization stress. The iv infusion of AVP (1 micrograms/kg/h) to chronically cannulated rats induced a fall of plasma T levels. A dose-dependent inhibition of plasma T values was also observed 3 h after ip administration of AVP (1, 5, 25 micrograms/kg) in animals killed by decapitation. An antagonist of AVP pressor activity [1-(beta-mercapto-beta 1 beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] AVP, antagonized, when injected ip at a dose of 30 micrograms/kg, the T-inhibitory effects of 3 h of immobilization stress. No consistent changes in plasma LH levels were observed in these experiments. To further evaluate the role of AVP in stress-induced T inhibition, AVP-deficient Brattleboro rats were submitted to 2 or 3 h of immobilization stress concomitantly with rats of the original Long-Evans strain. After 2 h and even more after 3 h of stress, plasma T levels fell in Long-Evans rats together with basal and human CG- or cAMP-stimulated T production by Percoll purified Leydig cells. In Brattleboro rats, 2 h of stress had no effects on plasma T levels nor in vitro basal or stimulated T production, whereas 3 h of immobilization were as effective as in Long-Evans animals. These results suggest, therefore, that at least part of T inhibitory effects of immobilization, those occurring during the first 2 h of stress, are due to an AVP-induced, post-cAMP blockade of T biosynthesis. Since plasma corticosterone, during 2 h of stress, rose to similar, albeit smaller, levels in Brattleboro rats as compared to those in Long-Evans animals, this glucocorticoid does not seem to be involved in the testicular effects of stress.(ABSTRACT TRUNCATED AT 400 WORDS)