Fluid inhibition as a factor in estrogen-induced increase of prostatic weight in castrated rats.

The mechanism by which estrogens inhibit castration atrophy has been investigated morphologically and biochemically utilizing ventral prostate from Copenhagen rats. The suppression of weight loss and gross edematous appearance of the prostate associated with the in vivo effect of 17 beta-estradiol (E2) could not be accounted for by DNA and protein synthesis. Increase in the fluid content in the tissues was confirmed by demonstration of significant increase in the ratio of wet/dry tissue weights. Light microscopy demonstrated that the main effects were on the stroma, characterized by large interglandular areas almost totally devoid of collagen resulting in an edematous appearance. Electron microscope studies showed an abundance of fluid localized adjacent to the capillary endothelium and some red blood cells indicating disturbances in capillary permeability. The combination of a prolactin secretion inhibiting agent with E2 alone, indicating an involvement of prolactin the estrogen effect. Differences in blood prolactin concentration between the strains of rats may influence the sensitivity of the prostate to estrogens.