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Abstract
The direct effects of gonadotropin releasing hormone (GnRH) upon testicular function include a rapid (integral of 20 min) receptor-mediated increase in phosphatidylinositol (PI) turnover. Incubation of rat interstitial cells with the super-agonist [D-Ala6]desGly10-GnRH N ethylamide (GnRHa) resulted in increased incorporation of [32P]Pi into PI (2-fold at 20 min). The effect on phospholipid turnover was followed by increased prostaglandin E (PGE) and testosterone production (3 h; with ED50 values of 0.5 and 0.75 nM respectively). It is concluded that increased PI turnover and PGE production might be involved in mediating the direct testicular effects of GnRH and its agonists.
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