Why the study?
Inducible nitric oxide synthase can be upregulated under conditions of increased oxidative stress with potential detrimental vascular effects, while cardioprotective endothelial nitric oxide is reduced in prehypertensive non-Hispanic Whites and non-Hispanic Blacks.
Does inhibition of iNOS improve endothelial NO-dependent vasodilation in prehypertensive non-Hispanic Whites and normotensive/prehypertensive non-Hispanic Blacks?
Does inhibition of iNOS improve endothelial NO-dependent vasodilation in prehypertensive non-Hispanic Whites and normotensive/prehypertensive non-Hispanic Blacks?
Inhibition of iNOS improves endothelial NO-dependent vasodilation in prehypertensive Whites and normotensive/prehypertensive Blacks, suggesting a potential target for improving vascular function.
Answers are grounded in this paper and cite their sources.
iNOS inhibition may enhance endothelial function in prehypertension; hypothesis-generating and requires randomized confirmation before clinical consideration.
Inducible nitric oxide synthase (iNOS) is typically upregulated in conditions of increased oxidative stress and may have detrimental effects on the vasculature. Endothelial nitric oxide (NO), which is cardioprotective, is reduced in prehypertensive non-Hispanic Whites and in non-Hispanic Blacks. We found that inhibition of iNOS can increase endothelial NO-dependent vasodilation in prehypertensive White participants and in both normotensive and prehypertensive Black participants.Inducible nitric oxide (NO) synthase (iNOS) can be upregulated under conditions of increased oxidative stress and may have detrimental effects on the vasculature. Endothelial NO, which is cardioprotective, is reduced in prehypertensive non-Hispanic Whites and in non-Hispanic Blacks. We found that inhibition of iNOS can increase endothelial NO-dependent vasodilation in prehypertensive White participants and in both normotensive and prehypertensive Black participants.
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Miller et al. (2020) studied this question.
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