ABSTRACT
Prolactin (PRL) mystifies the investigator by its seemingly multiple effects on prostatic physiology. There are specific PRL receptors in interstitial tissue of the testis. PRL deficiency results in depletion of receptors for both PRL and luteinizing hormone and produces testicular atrophy. Significant acceleration by PRL of growth of both ventral and dorsal lobes of the prostates of castrated and castrated-adrenalectomized immature rats, and by monolayers of human benign prostatic hyperplasia epithelium, show some growth-promoting potential which is independent of steroid. The human prostate is a heterogenous organ, both morphologically and biochemically and as such, sustains distinctive normal and pathological growth processes within its various regions. There are two ongoing research efforts which may prove of critical relevance to PRL/ prostate interactions. These are isolation of prostate-derived growth factor and thyrotrophin-releasing hormone analogs from human prostate. In 1965, M. Asano reported that total prostatectomy of male rats resulted in a significant increase in content and release of PRL from operated animals.
