The role of angiotensin-converting enzyme in the rat epididymis

• Published in: Journal of endocrinology Vol. 125; no. 3; pp. 457 - 465
• Main Authors: WONG, P. Y. D, UCHENDU, C. N
• Format: Journal Article
• Language: English
• Published: Colchester BioScientifica 01.06.1990; Portland Press
• Subjects: Angiotensin I - analysis; Angiotensin I - blood; Angiotensin II - analysis; Angiotensin II - blood; Animals; Biological and medical sciences; Body Fluids - analysis; Captopril - pharmacology; Epididymis - metabolism; Epididymis - physiology; Fertility - drug effects; Fundamental and applied biological sciences. Psychology; Hormone metabolism and regulation; Male; Mammalian male genital system; Orchiectomy; Peptidyl-Dipeptidase A - analysis; Peptidyl-Dipeptidase A - blood; Peptidyl-Dipeptidase A - physiology; Rats; Rats, Inbred Strains; Renin-Angiotensin System - physiology; Vertebrates: reproduction; Rat; Angiotensin I; Enzyme; Rodentia; Peptide hormone; Male genital system; Vertebrata; Epididymis; Mammalia; Enzymatic activity; Radioimmunoassay; Angiotensin converting enzyme; Angiotensin II
• ISSN: 0022-0795; 1479-6805
• DOI: 10.1677/joe.0.1250457

ABSTRACT In order to investigate the role of renin angiotensin in the epididymis, angiotensin-converting enzyme (ACE) activity and angiotensin I (AI) and angiotensin II (AII) concentrations were measured in the male reproductive tract and blood serum of the rat. High ACE activity was detected in the rat epididymis, with a major part of the activity being associated with epididymal spermatozoa. When spermatozoa were prevented from entering the epididymis by efferent duct ligation, the ACE activity in the epididymis was greatly reduced. The epithelial cells lining the epididymal duct were also shown to possess ACE activity which was dependent upon circulating androgens. Treatment of male rats with captopril at a single oral dose (20 mg/kg) significantly inhibited the ACE activity in the blood serum but had no effect on the activity of the epididymal fluid. The intraluminal ACE was protected from the circulating captopril by the blood–epididymis barrier. Long-term treatment with captopril (20 mg/kg per day, 8 weeks), however, caused an increase in blood serum ACE activity but was without effect on intraluminal ACE. The fertility and fecundity of male rats after treatment were apparently normal. The concentrations of AI and AII were high in the epididymal plasma and epididymal cell when compared with the respective concentrations in blood serum. The intraluminal AII concentration found (13 nmol/l) was close to the threshold concentrations that stimulate anion (and fluid) secretion in cultured epididymal epithelium in vitro. The high intraluminal AII concentration could not have been derived from the testicular fluid or spermatozoa since the rete testis fluid and sperm contained little AII. When spermatozoa were prevented from entering the epididymis by efferent duct ligation, the AII concentration of the epididymal plasma was almost completely abolished, indicating that intraluminal AII was formed endogenously in the epididymal lumen by sperm ACE. We propose that ACE released by epididymal spermatozoa converts AI (formed from the epididymal epithelial cells) to AII which plays a paracrine role in regulating electrolyte and fluid transport through apical membrane angiotensin receptors. Journal of Endocrinology (1990) 125, 457–465