The renin angiotensin system (RAS) has been shown to have tissue-related functions that are distinct from its systemic roles. We showed that angiotensin II type 1 (AT₁) receptors are present in mammalian sperm, and angiotensin II stimulates sperm motility, and capacitation. In addition, angiotensin II is present in human seminal plasma at concentrations higher than found in blood.

In testing the possibility that the prostate may be the source of seminal plasma angiotensin II, mRNA coding for angiotensinogen, (pro)renin and angiotensin converting enzyme were identified by RT-PCR in rat and human prostate and in prostate LNCaP cells, as well as the angiotensin receptors types 1 and 2 (AT₁ and AT₂) in human tissues, and AT₁ in rat. In human tissue, immunocytochemistry showed cellular co-localization of renin with the AT₁ receptor in secretory epithelial cells. Confirmation of the capacity of the prostate to secrete angiotensin II was shown by the detection of immunoreactive angiotensin in media removed from rat prostate organ cultures and LNCaP cells. Rat prostate angiotensin secretion was enhanced by dihydrotestosterone, but LNCaP angiotensin was stimulated by estradiol. This stimulation was blocked by tamoxifen.

Rat prostate AT₁ receptor expression was much greater in prepuberal than in postpuberal rats, but was not affected by a low sodium diet. It was however significantly enhanced by captopril pretreatment. These findings all suggest the independence of prostate and systemic RAS regulation. The data presented here suggest, that the prostate may be a source of the secreted angiotensin II found in seminal plasma.