Characterization of the Effects of Various Drugs Likely to Affect Smooth Muscle Tension on Isolated Human Seminal Vesicle Tissue

ObjectivesTo investigate the effects of different classes of drugs on the isometric tension of isolated human seminal vesicle (SV) tissue. The contractility of human SV contributes to the process of seminal emission during ejaculation. Different endogenous compounds, such as serotonin (5-HT), adenosine triphosphate (ATP), and nitric oxide, have been suggested to be involved in the control of contraction and relaxation of human SV smooth muscle. However, only limited data are available regarding the effects of compounds known to affect smooth musculature on SV contractile activity.MethodsUsing the organ bath technique, the effects of increasing concentrations (10 nm-1 μm/10 μm) of norepinephrine (NE), phenylephrine, endothelin 1, ATP, and 5-HT on human SV tissue at basal tension were studied. In another set-up, SV strip preparations were preincubated with prazosin (α-adrenergic blocker), nifedipine and verapamil (Ca2+-channel blockers), 2-aminoethoxydiphenyl borate [inositol 1,4,5-trisphosphate (IP3) antagonist], cromakalim (K+-channel opener), or Y-27632 (ROK inhibitor) (1 μm each, for 10 minutes), followed by the application of NE (0.1 μM, 1 μM, and 10 μm).ResultsSV smooth muscle was most effectively contracted by NE (mean = 75% of calibrated scale), phenylephrine (mean = 82% of calibrated scale), and endothelin 1 (mean = 70% calibrated scale), whereas only minor responses to ATP (mean = 10.65% calibrated scale) and 5-HT (mean = 6.3% calibrated scale) were observed. The contraction induced by NE was significantly inhibited after pre-exposure of the tissue to prazosin (−92.4%), cromakalim (−83.7%), 2-aminoethoxydiphenyl borate (−43.1%), Y-27632 (−42.8%), and nifedipine (−32.7%).Conclusionsα-adrenoceptor antagonism, activation of potassium channels, and inhibition of Rho-kinase decrease the sympathetic contraction of SV smooth muscle. This might be of significance with regard to the identification of new pharmacologic avenues to affect the male ejaculatory system.