Veijola M, Rajaniemi H
Mol Cell Endocrinol. 1986 May;45(2-3):113-8. doi: 10.1016/0303-7207(86)90138-3.
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.
通过向大鼠睾丸注射人绒毛膜促性腺激素（hCG，0.1 - 100 ng）与睾丸间质液（150 μl）或仅注射间质液（对照），并测量静脉注射的[125I]hCG的摄取量和睾丸中的间质液体积，研究了hCG增加大鼠睾丸血管通透性的机制。这两个参数在注射1 ng hCG时就已增加，在注射2 ng hCG时达到最大值。与hCG一起注射1000倍过量的去糖基化hCG并不能抑制hCG的作用。在生理盐水中或大鼠血清中注射2 ng hCG后未见增加。该反应对促黄体激素具有特异性，因为只有大鼠促黄体激素（rLH）能模拟hCG的作用，而去糖基化hCG、大鼠促卵泡激素（rFSH）或大鼠催乳素则不能。对间质液进行变性处理或向间质液中添加丝氨酸蛋白酶抑制剂（对氨基苯甲脒）可阻止hCG的作用。用抗hCGγ球蛋白琼脂糖处理经hCG激活的间质液并不能消除该间质液的通透性作用。这一点，以及hCG在间质液孵育过程中未被分解代谢的发现，表明hCG本身在间质液中不会转化为血管活性化合物。这些结果强烈表明，促黄体激素激活了大鼠睾丸液中的一种因子，该因子介导了它们的通透性作用。这种假定的因子似乎对热敏感，分子量超过10 000 Da。
