The possible mediation by steroids, prostaglandins or protein synthesis on the hCG-induced increase in hormone uptake and interstial fluid volume in the rat testis in vivo was studied following a single iv injection of hCG. A high dose of hCG increased its own uptake in the testis and this uptake coincided with an increase in capillary permeability and accumulation of interstial fluid. The possible role of steroids, prostaglandins and protein synthesis in these changes was studied in vivo using aminoglutethimide, indomethacin and cycloheximide, respectively, as inhibitors. However, none of these prevented the hCG-induced changes in uptake and interstial fluid volume, which suggests that they do not mediate this phenomenon.
An intratesticular injection of hCG (5 ng) mixed with testicular interstitial fluid (IF) increases vascular permeability in the rat testis. The present results show that the permeability increase induced by this treatment is accompanied by a massive accumulation of polymorphonuclear leucocytes (PMNs) in both the testicular postcapillary venules and the interstitium. Depletion of neutrophils in the circulation by treatment with anti-neutrophil serum significantly inhibited the permeability increase induced by this treatment. An intratesticular injection of PMNs (10(7) cells) or hCG alone had no effect on permeability, but a combination of the two caused a significant increase in permeability. The PMNs were found to secrete a component in vitro which, when injected intratesticularly together with hCG, caused a increase and a simultaneous massive accumulation of PMNs in the postcapillary venules and interstitium. This permeability increase was prevented by the serine protease inhibitor p-aminobenzamidine, suggesting an involvement of the plasminogen activator system in the response. The results suggest that hCG interacts with an IF component to produce leucotactic factors that increase permeability indirectly by attracting PMNs to the tissue, and that the IF component may originate in the PMNs.
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