Delay of castration induced regression in rat prostate by pituitary homografts

Although prolactin has a synergistic effect with testosterone in stimulating growth of the lateral lobe of the rat prostate, the role of prolactin in the absence of testosterone has not been well established. We studied the effect of prolactin on the rate of prostatic regression induced by castration in mature Sprague-Dawley rats. Anterior pituitaries from female rats were transplanted under the renal capsule in all rats. Castration and unilateral nephrectomy were carried out 1 week later. Half of the animals had the normal, non-grafted kidney removed and another half had the kidney bearing the pituitary grafts excised. Rats were sacrificed on days 0, 7, 10 and 14 and 3 lobes of the prostate were dissected separately. The lateral lobe showed a marked decrease in the rate of regression in the pituitary graft-bearing rats. In control animals, the relative weight of the lateral lobe on days 7, 10 and 14 was 38 ± 2% (mean ± SE), 33 ± 2% and 26 ± 2% of the day 0 value, respectively; the respective relative weight in animals carrying pituitary grafts was 67 ± 4%, 51 ± 5%, and 38 ± 3% of the day 0 value. The difference in the weight of the lateral lobe between the 2 groups was significant on days 7 (p < 0.01) and 10 (p < 0.05) and was not significant on day 14. There was no difference in the mean body weight in graft bearing and non-graft bearing animals. Bilateral adrenalectomy at the time of castration did not influence the rate of prostatic regression in either group. Furthermore, pituitaries implanted in rats castrated for 3 weeks had no stimulatory effect on the prostates. These results indicate that increased endogenous prolactin, in the absence of testicular and adrenal secretions, delays the castration-induced regression of the lateral lobe of the prostate of Sprague-Dawley rats.