Glu298Asp endothelial nitric oxide synthase polymorphism is a risk factor for erectile dysfunction in the Mexican mestizo population

Haydee Rosas-Vargas, Ramon M. Coral-Vazquez, Rosario Tapia, Jose L. Borja, Ricardo A. Salas, Fabio Salamanca

Research output: Contribution to journalArticle

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Abstract

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.
Original languageAmerican English
Pages (from-to)728-732
Number of pages5
JournalJournal of Andrology
DOIs
StatePublished - 1 Jan 2004
Externally publishedYes

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Nitric Oxide Synthase Type III
Erectile Dysfunction
Peptidyl-Dipeptidase A
Population
Nitric Oxide
Penile Erection
Cyclic GMP
Angiotensins
Genetic Predisposition to Disease
Renin-Angiotensin System
Vasodilator Agents
Vascular Smooth Muscle
Heart Diseases
Diabetes Mellitus
Research Design
Logistic Models
Smoking
Alleles
Odds Ratio
Regression Analysis

Cite this

Rosas-Vargas, Haydee ; Coral-Vazquez, Ramon M. ; Tapia, Rosario ; Borja, Jose L. ; Salas, Ricardo A. ; Salamanca, Fabio. / Glu298Asp endothelial nitric oxide synthase polymorphism is a risk factor for erectile dysfunction in the Mexican mestizo population. In: Journal of Andrology. 2004 ; pp. 728-732.
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abstract = "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.",
author = "Haydee Rosas-Vargas and Coral-Vazquez, {Ramon M.} and Rosario Tapia and Borja, {Jose L.} and Salas, {Ricardo A.} and Fabio Salamanca",
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Glu298Asp endothelial nitric oxide synthase polymorphism is a risk factor for erectile dysfunction in the Mexican mestizo population. / Rosas-Vargas, Haydee; Coral-Vazquez, Ramon M.; Tapia, Rosario; Borja, Jose L.; Salas, Ricardo A.; Salamanca, Fabio.

In: Journal of Andrology, 01.01.2004, p. 728-732.

Research output: Contribution to journalArticle

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 - 2004/1/1

Y1 - 2004/1/1

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.

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