L-Homoarginine and L-arginine are antagonistically related to blood pressure in an elderly population

Zwan, Leonard P. van der; Davids, Mariska; Scheffer, P; Dekker, Joost; Stehouwer, Coen D. A.; Teerlink, Tom

doi:10.1097/hjh.0b013e32836037fb

Cited by 48 publications

(29 citation statements)

References 43 publications

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“…It is notable that in contrast to the inverse associations between homoarginine and adverse cardiovascular outcome, we observed positive associations between circulating homoarginine and multiple CVD risk factors, including hypertension, obesity, insulin resistance, and dyslipidemia (Tables I and II in the online-only Data Supplement). Although an explanation for these apparently contradictory findings is still lacking, they are concordant with recent results obtained from the Hoorn Study, in which, despite a strong positive correlation of circulating homoarginine with systolic and diastolic blood pressure, 29 low plasma homoarginine emerged as an independent predictor for all-cause and cardiovascular mortality. 27 One possible explanation for these findings is that homoarginine increases in response to risk factors, such as obesity or hypertension but then attenuates, to some extent, their adverse cardiovascular influence.…”

Section: Discussionsupporting

confidence: 78%

Homoarginine and Cardiovascular Outcome in the Population-Based Dallas Heart Study

Atzler

Gore

Ayers

et al. 2014

ATVB

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Plasma homoarginine and outcomes data were available for 3514 DHS participants. The cohort consisted of 56% women; the median age of the cohort was 43 (interquartile range, 36-52) years. The study comprised 52% blacks, 29% whites, and 17% Hispanics. Median plasma homoarginine was 2.80 (interquartile range, 2.14-3.54) μmol/l. The baseline © 2014 American Heart Association, Inc. Objective-The nonproteinogenic amino acid homoarginine has been postulated to have antiatherosclerotic effects as a weak substrate of nitric oxide synthase. This investigation in the population-based Dallas Heart Study (DHS) aimed to evaluate the association of homoarginine with clinical and subclinical cardiovascular outcomes. Approach and Results-Plasma homoarginine was measured in 3514 participants of the DHS using liquid chromatographytandem mass spectrometry. Associations between homoarginine and major adverse cardiovascular events and all-cause mortality were analyzed using Cox proportional hazard models adjusting for cardiovascular risk factors. linear regression was used to assess cross-sectional associations between homoarginine and subclinical cardiovascular disease, including coronary artery calcium measured by electron beam-computed tomography, and aortic plaque burden and aortic wall thickness by MRI. Median age was 43 (interquartile range, 36-52) years, with 56% women and 52% black participants. Median follow-up was 9.4 (9.0-9.8) years. Median plasma homoarginine was 2.80 (2.14-3.54) μmol/l. In multivariable models, higher homoarginine was associated with lower rate of major adverse cardiovascular events (hazard ratio, 0.86; 95% confidence interval, 0.75-0.98) and lower all-cause mortality (hazard ratio, 0.82; 0.73-0.92; per 1 log SD increase in homoarginine). Homoarginine was inversely and independently associated with aortic wall thickness (β-estimate, −0.04; P<0.01) but not with aortic plaque burden and coronary artery calcium. Conclusions-Homoarginine is inversely associated with subclinical vascular disease and with risk for cardiovascular disease events. Additional studies are needed to evaluate whether the regulation of plasma homoarginine could emerge as a novel therapeutic option to improve outcomes in cardiovascular disease.

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Section: Discussionsupporting

confidence: 78%

Homoarginine and Cardiovascular Outcome in the Population-Based Dallas Heart Study

Atzler

Gore

Ayers

et al. 2014

ATVB

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“…In turn, ornithine can be converted to l-citrulline, which is subsequently converted back to l-arginine to complete the urea cycle (Morris 1992). l-Homoarginine which competes with l-arginine as substrate for eNOS (Van der Zwan et al 2013) and NOS inhibitors such as asymmetric dimethylarginine (ADMA) (Böger 2005) and symmetric dimethylarginine (SDMA) (Siegerink et al 2013) are also important factors which determine NO synthesis capacity.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide synthesis capacity, ambulatory blood pressure and end organ damage in a black and white population: the SABPA study

et al. 2015

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Nitric oxide (NO) synthesis capacity is determined by the availability of substrate(s) such as L-arginine and the influence of nitric oxide synthase (NOS) inhibitors, asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA). These factors may be important in black South Africans with a very high prevalence of hypertension. We compared ambulatory blood pressure (BP), markers of end organ damage and NO synthesis capacity markers [L-arginine, L-homoarginine, L-citrulline, L-arginine:ADMA, ADMA, SDMA and dimethylarginine (DMA)], between black and white teachers (n = 390). Associations of nighttime BP and markers of end organ damage with NO synthesis capacity markers were also investigated. Although black men and women had higher BP and albumin-to-creatinine ratio (ACR) (all p < 0.001), they also had higher L-arginine, L-homoarginine, L-arginine:ADMA and lower SDMA and DMA levels (all p < 0.05). Only in white men ADMA concentrations associated positively with nighttime systolic blood pressure (R (2) = 0.20, β = 0.26, p = 0.009), nighttime diastolic blood pressure (R (2) = 0.23, β = 0.27, p = 0.007), carotid intima media thickness (cIMT) (R (2) = 0.36, β = 0.22, p = 0.008) and ACR (R (2) = 0.14, β = 0.32, p = 0.001). Our findings suggest that despite an adverse cardiovascular profile in blacks, their NO synthesis capacity profile seems favourable, and that other factors, such as NO inactivation, may prove to be more important.

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“…Recently, L-homoarginine has been shown to be associated with smoking status [34,35]. In our PAD patients, smokers also had significantly lower mean age-adjusted L-homoarginine levels compared to non-and ex-smokers.…”

Section: Odds Ratio (95%ci) P-valuementioning

confidence: 69%

Serum concentrations of l-arginine and l-homoarginine in male patients with intermittent claudication: A cross-sectional and prospective investigation in the CAVASIC Study

et al. 2015

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L-Homoarginine and L-arginine are antagonistically related to blood pressure in an elderly population

Abstract: In elderly participants, plasma levels of L-homoarginine and L-arginine are independently associated with clinically relevant differences in blood pressure in an antagonistic fashion.

Cited by 48 publications

References 43 publications

Homoarginine and Cardiovascular Outcome in the Population-Based Dallas Heart Study

Homoarginine and Cardiovascular Outcome in the Population-Based Dallas Heart Study

Nitric oxide synthesis capacity, ambulatory blood pressure and end organ damage in a black and white population: the SABPA study

Serum concentrations of l-arginine and l-homoarginine in male patients with intermittent claudication: A cross-sectional and prospective investigation in the CAVASIC Study

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