Abstract
Endogenous NO synthase inhibitors (end-NOSIs) have been associated with cardiovascular risk factors and atherosclerosis. In addition, end-NOSIs may directly cause hypertension through hemodynamic effects. We aimed to examine the association between end-NOSI asymmetrical dimethylarginine (ADMA) and N-guanidino-monomethyl-arginine (NMMA), subclinical atherosclerosis, and arterial hemodynamics. We studied 922 adults participating in a population-based study (PREVENCION Study) and examined the correlation between end-NOSI/L-arginine and arterial hemodynamics, carotid-femoral pulse wave velocity, and carotid intima-media thickness using linear regression. ADMA, NMMA, and L-arginine were found to be differentially associated with various classic cardiovascular risk factors. ADMA and NMMA (but not L-arginine) were significant predictors of carotid intima-media thickness, even after adjustment for cardiovascular risk factors, C-reactive protein, and renal function. In contrast, ADMA and NMMA did not predict carotid-femoral pulse wave velocity, blood pressure, or hemodynamic abnormalities. Higher L-arginine independently predicted systolic hypertension, higher central pulse pressure, incident wave amplitude, central augmented pressure, and lower total arterial compliance but not systemic vascular resistance or cardiac output. We conclude that ADMA and NMMA are differentially associated with cardiovascular risk factors, but both end-NOSIs are independent predictors of carotid atherosclerosis. In contrast, they are not associated with large artery stiffness, hypertension, or hemodynamic abnormalities. Our findings are consistent with a role for asymmetrical arginine methylation in atherosclerosis but not in large artery stiffening, hypertension, or long-term hemodynamic regulation. L-Arginine is independently associated with abnormal pulsatile (but not resistive) arterial hemodynamic indices, which may reflect abnormal L-arginine transport, leading to decreased intracellular bioavailability for NO synthesis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1051-1059 |
| Number of pages | 9 |
| Journal | Hypertension |
| Volume | 52 |
| Issue number | 6 |
| DOIs | |
| State | Published - Dec 2008 |
| Externally published | Yes |
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Keywords
- Arterial stiffness
- Asymmetrical dimethylarginine
- Atherosclerosis
- Hemodynamics
- Hypertension
ASJC Scopus subject areas
- Internal Medicine
Cite this
Endogenous nitric oxide synthase inhibitors, arterial hemodynamics, and subclinical vascular disease : The PREVENCION study. / Chirinos, Julio A.; David, Robert; Bralley, J. Alexander; Zea-Díaz, Humberto; Muñoz-Atahualpa, Edgar; Corrales-Medina, Fernando; Cuba-Bustinza, Carolina; Chirinos-Pacheco, Julio; Medina-Lezama, Josefina.
In: Hypertension, Vol. 52, No. 6, 12.2008, p. 1051-1059.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endogenous nitric oxide synthase inhibitors, arterial hemodynamics, and subclinical vascular disease
T2 - The PREVENCION study
AU - Chirinos, Julio A.
AU - David, Robert
AU - Bralley, J. Alexander
AU - Zea-Díaz, Humberto
AU - Muñoz-Atahualpa, Edgar
AU - Corrales-Medina, Fernando
AU - Cuba-Bustinza, Carolina
AU - Chirinos-Pacheco, Julio
AU - Medina-Lezama, Josefina
PY - 2008/12
Y1 - 2008/12
N2 - Endogenous NO synthase inhibitors (end-NOSIs) have been associated with cardiovascular risk factors and atherosclerosis. In addition, end-NOSIs may directly cause hypertension through hemodynamic effects. We aimed to examine the association between end-NOSI asymmetrical dimethylarginine (ADMA) and N-guanidino-monomethyl-arginine (NMMA), subclinical atherosclerosis, and arterial hemodynamics. We studied 922 adults participating in a population-based study (PREVENCION Study) and examined the correlation between end-NOSI/L-arginine and arterial hemodynamics, carotid-femoral pulse wave velocity, and carotid intima-media thickness using linear regression. ADMA, NMMA, and L-arginine were found to be differentially associated with various classic cardiovascular risk factors. ADMA and NMMA (but not L-arginine) were significant predictors of carotid intima-media thickness, even after adjustment for cardiovascular risk factors, C-reactive protein, and renal function. In contrast, ADMA and NMMA did not predict carotid-femoral pulse wave velocity, blood pressure, or hemodynamic abnormalities. Higher L-arginine independently predicted systolic hypertension, higher central pulse pressure, incident wave amplitude, central augmented pressure, and lower total arterial compliance but not systemic vascular resistance or cardiac output. We conclude that ADMA and NMMA are differentially associated with cardiovascular risk factors, but both end-NOSIs are independent predictors of carotid atherosclerosis. In contrast, they are not associated with large artery stiffness, hypertension, or hemodynamic abnormalities. Our findings are consistent with a role for asymmetrical arginine methylation in atherosclerosis but not in large artery stiffening, hypertension, or long-term hemodynamic regulation. L-Arginine is independently associated with abnormal pulsatile (but not resistive) arterial hemodynamic indices, which may reflect abnormal L-arginine transport, leading to decreased intracellular bioavailability for NO synthesis.
AB - Endogenous NO synthase inhibitors (end-NOSIs) have been associated with cardiovascular risk factors and atherosclerosis. In addition, end-NOSIs may directly cause hypertension through hemodynamic effects. We aimed to examine the association between end-NOSI asymmetrical dimethylarginine (ADMA) and N-guanidino-monomethyl-arginine (NMMA), subclinical atherosclerosis, and arterial hemodynamics. We studied 922 adults participating in a population-based study (PREVENCION Study) and examined the correlation between end-NOSI/L-arginine and arterial hemodynamics, carotid-femoral pulse wave velocity, and carotid intima-media thickness using linear regression. ADMA, NMMA, and L-arginine were found to be differentially associated with various classic cardiovascular risk factors. ADMA and NMMA (but not L-arginine) were significant predictors of carotid intima-media thickness, even after adjustment for cardiovascular risk factors, C-reactive protein, and renal function. In contrast, ADMA and NMMA did not predict carotid-femoral pulse wave velocity, blood pressure, or hemodynamic abnormalities. Higher L-arginine independently predicted systolic hypertension, higher central pulse pressure, incident wave amplitude, central augmented pressure, and lower total arterial compliance but not systemic vascular resistance or cardiac output. We conclude that ADMA and NMMA are differentially associated with cardiovascular risk factors, but both end-NOSIs are independent predictors of carotid atherosclerosis. In contrast, they are not associated with large artery stiffness, hypertension, or hemodynamic abnormalities. Our findings are consistent with a role for asymmetrical arginine methylation in atherosclerosis but not in large artery stiffening, hypertension, or long-term hemodynamic regulation. L-Arginine is independently associated with abnormal pulsatile (but not resistive) arterial hemodynamic indices, which may reflect abnormal L-arginine transport, leading to decreased intracellular bioavailability for NO synthesis.
KW - Arterial stiffness
KW - Asymmetrical dimethylarginine
KW - Atherosclerosis
KW - Hemodynamics
KW - Hypertension
UR - http://www.scopus.com/inward/record.url?scp=57449121152&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57449121152&partnerID=8YFLogxK
U2 - 10.1161/HYPERTENSIONAHA.108.120352
DO - 10.1161/HYPERTENSIONAHA.108.120352
M3 - Article
C2 - 18852383
AN - SCOPUS:57449121152
VL - 52
SP - 1051
EP - 1059
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 6
ER -