Objective: Increasing evidence suggests that endothelial nitric oxide (NO) deficit and baroreflex dysfunction are associated with a variety of cardiovascular conditions, ranging from arterial hypertension to stroke and coronary heart disease, importantly appearing even in preclinical stages of the disease. To test the hypothesis that the arterial baroreflex has a modulatory effect on NO-dependent vasodilation, sodium nitroprusside (SNP), a spontaneous NO-donor, vasodilatory effect was studied in conjunction with sinocarotid baroreceptor magnetic stimulation and potential implementation in NO deficiency states.
Methods: Mean femoral artery blood pressure (MAP), heart rate (HR) and ear lobe skin microcirculatory blood flow, measured by a microphotoelectric plethysmogram (MPPG), were simultaneously recorded in conscious rabbits before and after 40-min sinocarotid baroreceptor exposure to 350 mT static magnetic field (SMF), generated by Nd2-Fe4-B alloy (n=8) or sham magnets (n=8, controls). Arterial baroreflex sensitivity (BRS) was measured by changes in HR and MAP (ΔHR/ΔMAP) after intravenous bolus injections of SNP and phenylephrine.
Results: The vasodilatory effect of SNP significantly increased after SMF sinocarotid baroreceptor exposure (MPPGbeforeSMF: 2.57 ± 0.81 V vs. MPPGafterSMF: 7.82 ± 1.61 V, p<0.0001) and positively correlated with significant increase in BRS (r=0.51, p=0.01).
Conclusions: Baroreflex-mediated increment in vessel sensitivity to NO is suggested to be a new mechanism in baroreflex physiology with potential implementation in cardiovascular conditions where NO deficit and autonomic dysfunction increase the risk of morbidity and mortality substantially.
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