A specific chemical cofactor called BH4 (tetrahydrobiopterin) may be the missing link to understanding and potentially reversing the decline in vascular health that occurs after menopause, according to a small study published January 13 in the American Journal of Physiology - Heart and Circulatory Physiology.
“These results provide novel insight into a potential mechanism by which oxidative stress contributes to the large elastic artery stiffening in estrogen-deficient postmenopausal women,” the authors write. BH4 is critical to the body’s process of producing nitric oxide. Nitric oxide increases arterial dilation and tone and decreases arterial stiffness.
BH4 was given to 24 postmenopausal and 9 premenopausal women. Three hours later. BH4 increased carotid artery compliance by 24±5% in the postmenopausal women (versus baseline, P<0.0001) but had no effect in the younger women (P=0.10) or on brachial artery compliance in either group (P=0.52). Similarly, it increased brachial artery flow-mediated dilation (FMD) 64±11% in the postmenopausal women (P<0.001) but did not have a significant effect in the premenopausal group (P=0.01).
In the second part of the study, half of the postmenopausal women were given placebo; the other half received transdermal estradiol. Two days later, women given estradiol had effects similar to the women who had received BH4, while those given placebo experienced no changes, even after adjusting for potential confounders. Further, coadministered BH4 and estradiol provided no further benefit on vascular function, suggesting that estrogen helps to maintain adequate BH4 levels.
“Our results suggest that the beneficial effects of estrogen on arterial stiffening in previously estrogen-deficient postmenopausal women may be mediated by improved endothelial vasodilatory tone, secondary to increasing BH4 bioavailability,” the authors write.
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