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1.
Andrology ; 3(5): 902-8, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26216079

ABSTRACT

Testosterone has been found to play important roles in men's sexual function. However, the effects of testosterone can be modulated by androgen receptor (AR) CAG repeat polymorphism. It could also contribute to the risk of erectile dysfunction (ED). The aim of this study is to evaluate the interaction of serum testosterone levels and AR CAG repeat polymorphism on the risk of ED in aging Taiwanese men. This cross-sectional data of Taiwanese men older than 40 years were collected from a free health screening held between August 2010 and August 2011 in Kaohsiung city, Taiwan. All participants completed a health questionnaires included five-item version of the International Index of Erectile Function (IIEF-5) and the International Prostate Symptoms Score, received a detailed physical examination and provided 20 cm3 whole blood samples for biochemical and genetic evaluation. The IIEF-5 was used to evaluate ED. Serum albumin, total testosterone (TT), and sex hormone-binding globulin levels were measured. Free testosterone level was calculated. AR gene CAG repeat polymorphism was determined by direct sequencing. Finally, 478 men with the mean age of 55.7 ± 4.8 years were included. When TT levels were above 330 ng/dL, the effect of testosterone level on erectile function seemed to reach a plateau and a significantly negative correlation between AR CAG repeat length and the score of IIEF-5 was found (r = -0.119, p = 0.034). After adjusting for other covariates, the longer AR CAG repeat length was still an independent risk factor for ED in subjects with TT above 330 ng/dL (p = 0.006), but not in TT of 330 ng/dL or below. In conclusion, both serum testosterone levels and AR CAG repeat polymorphism can influence erectile function concomitantly. In subjects with normal TT concentration, those with longer AR CAG repeat lengths have a higher risk of developing ED.


Subject(s)
Erectile Dysfunction/blood , Erectile Dysfunction/genetics , Receptors, Androgen/genetics , Testosterone/blood , Adult , Aged , Aged, 80 and over , Aging , Cross-Sectional Studies , Erectile Dysfunction/epidemiology , Humans , Male , Middle Aged , Polymorphism, Single Nucleotide , Risk Factors , Serum Albumin/analysis , Sex Hormone-Binding Globulin/metabolism , Surveys and Questionnaires , Taiwan/epidemiology
2.
Andrology ; 2(1): 59-64, 2014 Jan.
Article in English | MEDLINE | ID: mdl-24166981

ABSTRACT

Ejaculation is a process involving sympathetic and parasympathetic effects during different stages - emission and ejection. Some conditions of ejaculation dysfunction are associated with autonomic nerves. However, the exact effects of autonomic nerves on ejaculation are not well defined. Autonomic agonists induce different recorded trace patterns of seminal vesicular contraction. The different traces contain different components of phasic and tonic contraction, which may have physiological implications. In this study, we examined isolated rat seminal vesicle (SV) contraction by phenylephrine (PE), acetylcholine, and their respective antagonists and then speculated upon physiological roles of sympathetic and parasympathetic nerves on SV during ejaculation. We found that PE and Ach both achieved good contraction of rat SV. Compared to α1b for sympathetic and M1, M2 for parasympathetic receptors, α1a and M3 are the relatively dominant subtypes on rat SV. Adrenergic and cholinergic agonists cause different trace patterns of SV contraction. We speculated that the sympathetic effect is dominant during emission to squeeze seminal fluid out and that the parasympathetic effect is dominant during ejection to provide an anti-reflux effect on the ejaculatory duct.


Subject(s)
Ejaculation/physiology , Muscle, Smooth/innervation , Parasympathetic Nervous System/physiology , Seminal Vesicles/innervation , Sympathetic Nervous System/physiology , Acetylcholine/pharmacology , Adrenergic Agonists/pharmacology , Animals , Cholinergic Agonists/pharmacology , Male , Muscle Contraction/drug effects , Muscle Contraction/physiology , Phenylephrine/pharmacology , Rats , Rats, Wistar , Receptor, Muscarinic M1/physiology , Receptor, Muscarinic M2/physiology , Receptor, Muscarinic M3/physiology , Receptors, Adrenergic, alpha-1/physiology , Vasoconstrictor Agents/pharmacology , Vasodilator Agents/pharmacology
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