To the Editor: We read with great interest the article by Dr Dong and colleagues1 dealing with the relation ship between plasma total homocysteine levels and circadian blood pressure variation. The results of their study demonstrated that, in Chinese hypertensive adults who received ambulatory blood pressure monitoring, plasma total homocysteine levels in nondippers of nocturnal blood pressure were significantly higher than those in dippers. It was also shown that plasma total homocysteine levels inversely correlated with the fall in nocturnal systolic and diastolic blood pressure. Multivariate logistic regression analysis identified that plasma total homocysteine might be an independent factor which correlated with the presence of nondipping blood pressure status in hypertensive adults. In addition, the percentage of dipping blood pressure status was higher, and the percentage of nondipping blood pressure status was lower in subjects with CC/CT genotypes of the methylenetetrahydrofolate reductase than in subjects with TT genotype. The authors have proposed that high plasma total homocysteine levels might be associated with disturbed circadian blood pressure variation in Chinese hypertensive adults. Evidence indicates that endothelial function might have a crucial role in circadian blood pressure rhythm. Rekhviashvili et al.2 demonstrated that nondipper circadian blood pressure rhythm was associated with the significant impairment of endothelial function. It has been shown that endothelium-dependent vasodilation was blunted through a lesser nitric oxide release in nondippers compared with patients who have dipper hypertension.3 On the other hand, homocysteine has been shown to be associated with endothelial dysfunction. Tawakol et al.4 demonstrated that endothelium-dependent vasodilation was impaired in subjects with elevated plasma homocysteine. We reported that increased levels of plasma total homocysteine levels were associated with decreased levels of plasma nitric oxide-metabolite concentration, suggesting that hyperhomocysteinemia could be accompanied by reduced nitric oxide-production.5 It has been implicated that folate may be the important determinant of plasma homocysteine concentration in subjects with cardiovascular diseases.6 Recently, Li et al.7 have observed that the methylenetetrahydrofolate reductase A1298C mutation accompanied by hyperhomocysteinemia was associated with elevated diastolic blood pressure in a Chinese hypertensive population. Because folate treatment might normalize nitric oxide synthase-dependence of vascular tone in the metabolic syndrome,8 it is strongly speculated that folate/homocysteine status would substantively affect endothelial function in subjects with hypertension and cardiometabolic disorders. Therefore, we would like to know whether endothelial function might be related to plasma homocysteine levels, methylenetetrahydrofolate reductase polymorphism, and circadian blood pressure variation in the study of Dr Dong and colleagues. Since the nondipper circadian pattern of blood pressure has been linked to a higher risk of cerebrovascular and cardiovascular complications,2 it would be important to assess more precisely the possible links among plasma homocysteine levels, methylenetetrahydrofolate reductase polymorphism, circadian blood pressure variation and endothelial dysfunction, and their contribution to the progression of the target organ damage in hypertensive subjects. DISCLOSURE The authors declared no conflict of interest. REFERENCES 1. Dong YF, Zhan BM, Hao QY, Ruan ZH, Xu ZX, Deng M, Chen DW, Zou YQ, Chen J, Li P, Cheng XS. Plasma homocysteine levels are associated with circadian blood pressure variation in Chinese hypertensive adults. Am J Hypertens 2017; 30: 1203– 1210. Google Scholar CrossRef Search ADS PubMed 2. Rekhviashvili A, Giorgobian T, Minashvili A, Baganasgvili E. Influence of circadian blood pressure profile on endothelial function in patients with and without arterial hypertension. Georgian Med News 2015; 240: 29– 32. 3. Higashi Y, Nakagawa K, Kimura M, Noma K, Hara K, Sasaki S, Goto C, Oshima T, Chayama K, Yoshizumi M. Circadian variation of blood pressure and endothelial function in patients with essential hypertension: a comparison of dippers and non-dippers. J Am Coll Cardiol 2002; 40: 2039– 2043. Google Scholar CrossRef Search ADS PubMed 4. Tawakol A, Omland T, Gerhard M, Wu JT, Creager MA. Hyperhomocyst(e)inemia is associated with impaired endothelium-dependent vasodilation in humans. Circulation 1997; 95: 1119– 1121. Google Scholar CrossRef Search ADS PubMed 5. Tsuda K. Hyperhomocysteinemia and membrane fluidity of red blood cells in normotensive and hypertensive men: an electron paramagnetic resonance investigation. Clin Exp Pharmacol Physiol . 2007; 34: S70– S72. Google Scholar CrossRef Search ADS 6. Lee BJ, Lin PT, Liaw YP, Chang SJ, Cheng CH, Huang YC. Homocysteine and risk of coronary artery disease: folate is the important determinant of plasma homocysteine concentration. Nutrition 2003; 19: 577– 583. Google Scholar CrossRef Search ADS PubMed 7. Li WX, Liao P, Hu CY, Cheng F, Zhang T, Sun YY, Tang L, Wang MM, Liu KS, Liu D, Liu F. Interactions of methylenetetrahydrofolate reductase gene polymorphisms, folate, and homocysteine on blood pressure in a Chinese hypertensive population. Clin Lab 2017; 63: 817– 825. Google Scholar PubMed 8. Schneider MP, Schlaich MP, Harazny JM, Raff U, Ritt M, Ott C, Schmieder RE. Folic acid treatment normalizes NOS-dependence of vascular tone in the metabolic syndrome. Obesity (Silver Spring) 2011; 19: 960– 967. Google Scholar CrossRef Search ADS PubMed © American Journal of Hypertension, Ltd 2018. All rights reserved. For Permissions, please email: email@example.com
American Journal of Hypertension – Oxford University Press
Published: Apr 1, 2018
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