TY - JOUR
T1 - Glu298Asp endothelial nitric oxide synthase polymorphism is a risk factor for erectile dysfunction in the Mexican mestizo population
AU - Rosas-Vargas, Haydee
AU - Coral-Vazquez, Ramon M.
AU - Tapia, Rosario
AU - Borja, Jose L.
AU - Salas, Ricardo A.
AU - Salamanca, Fabio
PY - 2004
Y1 - 2004
N2 - Penile erection depends on the balanced action between antagonist vasoactive molecules such as nitric oxide (NO) and angiotensin. Endothelial nitric oxide synthase (eNOS) and angiotensin-converting enzyme (ACE) polymorphisms have been associated with endothelial dysfunction, which is described as a cause of erectile dysfunction (ED). Endothelial NOS and ACE are both regulators of vascular and corporal smooth muscle tone, which are connected by interaction between the NO-cyclic guanosine monophosphate pathway and the renin-angiotensin system. We analyzed the frequencies of 894 G/T (Glu298Asp) eNOS and ACE I/D polymorphisms in Mexican patients with ED (n = 53) and in an age-matched control group (n = 62). The populations analyzed were in Hardy Weinberg equilibrium. We found significant differences in allelic (X2 = 4.42; P = .03) and genotypic frequencies (X2 = 3.96; P = .04) between patients and controls for the 894 G/T eNOS polymorphism. Presence of the 894T allele in carriers increased the risk of ED (odds ratio [TT + GT versus GG] = 2.37; 95% confidence interval, 1.08 to 5.21; P = .02). Multiple logistic regression analysis showed that the Glu298Asp polymorphism was an independent factor for ED, as was diabetes mellitus, hypertension, cardiac disease, and cigarette smoking. No association was found between ACE I/D polymorphism and ED in the population studied. Therefore, our results suggest that Glu298Asp eNOS polymorphism plays a role as a genetic susceptibility factor for ED.
AB - Penile erection depends on the balanced action between antagonist vasoactive molecules such as nitric oxide (NO) and angiotensin. Endothelial nitric oxide synthase (eNOS) and angiotensin-converting enzyme (ACE) polymorphisms have been associated with endothelial dysfunction, which is described as a cause of erectile dysfunction (ED). Endothelial NOS and ACE are both regulators of vascular and corporal smooth muscle tone, which are connected by interaction between the NO-cyclic guanosine monophosphate pathway and the renin-angiotensin system. We analyzed the frequencies of 894 G/T (Glu298Asp) eNOS and ACE I/D polymorphisms in Mexican patients with ED (n = 53) and in an age-matched control group (n = 62). The populations analyzed were in Hardy Weinberg equilibrium. We found significant differences in allelic (X2 = 4.42; P = .03) and genotypic frequencies (X2 = 3.96; P = .04) between patients and controls for the 894 G/T eNOS polymorphism. Presence of the 894T allele in carriers increased the risk of ED (odds ratio [TT + GT versus GG] = 2.37; 95% confidence interval, 1.08 to 5.21; P = .02). Multiple logistic regression analysis showed that the Glu298Asp polymorphism was an independent factor for ED, as was diabetes mellitus, hypertension, cardiac disease, and cigarette smoking. No association was found between ACE I/D polymorphism and ED in the population studied. Therefore, our results suggest that Glu298Asp eNOS polymorphism plays a role as a genetic susceptibility factor for ED.
KW - Angiotensin-converting enzyme
KW - Endothelial dysfunction
KW - Impotence
UR - http://www.scopus.com/inward/record.url?scp=4143075936&partnerID=8YFLogxK
U2 - 10.1002/j.1939-4640.2004.tb02847.x
DO - 10.1002/j.1939-4640.2004.tb02847.x
M3 - Artículo
SN - 0196-3635
VL - 25
SP - 728
EP - 732
JO - Journal of Andrology
JF - Journal of Andrology
IS - 5
ER -