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Effects of Silodosin and Tamsulosin on the Seminal Vesicle Contractile Response
Author(s) -
HAYASHI Tokumasa,
TAKEYA Mitsue,
NAKAMURA Keiichiro,
MATSUOKA Kei
Publication year - 2016
Publication title -
luts: lower urinary tract symptoms
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.451
H-Index - 15
eISSN - 1757-5672
pISSN - 1757-5664
DOI - 10.1111/luts.12072
Subject(s) - silodosin , tamsulosin , tetrodotoxin , seminal vesicle , ejaculation , stimulation , antagonist , medicine , nifedipine , inhibitory postsynaptic potential , endocrinology , chemistry , anesthesia , receptor , prostate , calcium , lower urinary tract symptoms , cancer , hyperplasia
Objectives To understand the mechanisms underlying ejaculation dysfunction caused by α 1A ‐adrenocetor ( AR ) antagonists, the effects of α 1A ‐AR antagonists on the contractile responses of the seminal vesicle were investigated. Methods Isolated seminal vesicles from guinea pigs were cannulated and pressurized, and the changes in the intraluminal pressure were recorded. Periodic applications of electrical stimulation ( ES ) caused biphasic increase in the intraluminal pressure, that is, initial and subsequent contractions. The effects of silodosin and tamsulosin, α 1A ‐AR antagonists, on the contractile responses were examined. Results The ES ‐induced biphasic contractions were blocked by tetrodotoxin ( TTX ). Silodosin and tamsulosin suppressed the initial contractions in a dose‐dependent manner, while also exerting various inhibitory effects on the subsequent contractions. Increases in the intraluminal pressure facilitated spontaneous phasic contractions. The spontaneous contractions were not affected by TTX or α 1A ‐AR antagonists, but were abolished by nifedipine. Conclusions The initial contractions triggered by neuronal excitations were suppressed by silodosin and tamsulosin, suggesting that the ejaculation dysfunction may be attributed to the α 1A ‐AR antagonist‐mediated suppression of nerve‐evoked contractions in the seminal vesicle. The subsequent contractions may be induced by mechanical stimulation associated with the initial, nerve‐evoked contractions. Alternatively, other transmitters may be involved to various degrees in the neuromuscular transmission of the seminal vesicle.