Increasing evidence supports a role of the sympathetic nervous system – the “fight or flight” response – in the development of hypertension, particularly obesity-associated hypertension. Obesity also is associated with impaired modulation of vascular tone by endothelial cells and the signaling molecule nitric oxide, which also contributes to blood pressure regulation.
Alfredo Gamboa, M.D., MSCI, and colleagues explored a possible interaction between sympathetic activity and nitric oxide function in obese hypertensive subjects.
They found that with intact autonomic nervous system activity, nitric oxide-mediated vasodilation was blunted compared with endothelial independent vasodilation. Sympathetic nervous system blockade restored the nitric oxide-mediated vasodilation.
The results, reported in the journal Hypertension, support the concept that increased sympathetic activity contributes to endothelial dysfunction and impaired response to nitric oxide. The findings provide a rationale for targeting sympathetic activation in the treatment of obesity-associated hypertension.
This research was supported in part by grants from the National Institutes of Health (HL095905, HL056693, RR024975).
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