Luteinising hormones activate a factor(s) in testicular interstitial fluid which increases testicular vascular permeability.

The mechanism by which hCG increases the rat testicular vascular permeability was studied by injecting the testes with hCG (0.1-100 ng) together with testicular interstitial fluid (150 mul) or with the fluid alone (control) and measuring the uptake of i.v. injected [125I]hCG and the interstitial fluid volume in the testes. Both parameters were already increased with 1 ng of hCG and maxima were seen with 2 ng of hCG. The effect of hCG was not inhibited by injection of a 1000-fold excess of deglycosylated hCG together with hCG. No increase was seen after injection of 2 ng of hCG in saline or in rat serum. The response was specific to luteinising hormones since only rLH mimicked the effect of hCG, but deglycosylated hCG, rFSH or rat prolactin did not. Denaturation of the fluid or addition of serine protease inhibitor (p-aminobenzamidine) to the fluid prevented the effect of hCG. Treatment of the hCG-activated fluid with anti-hCG gamma-globulin Sepharose did not abolish the permeability effect of the fluid. This, and the finding that hCG is not catabolised during incubation in the fluid, suggests that hCG itself is not transformed to a vasoactive compound in the fluid. These results strongly suggest that luteinising hormones activate a factor(s) in rat testicular fluid which mediates their permeability effect. The putative factor(s) seems to be heat-sensitive with a molecular weight of over 10 000 Da.