PP.12.10

Abstract

Objective: Increasing evidence suggests nitric oxide (NO) deficit and baroreflex dysfunction to be characteristic for a wide variety of cardiovascular conditions even in preclinical stages of the disease. 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. Design and method: Mean femoral artery blood pressure (MAP), heart rate (HR) and ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded in conscious rabbits before and after 40-min sinocarotid baroreceptors exposure to 350 mT static magnetic field (SMF), generated by Nd-Fe-B alloy (n = 8) or sham magnets (n = 8, controls). Arterial baroreflex sensitivity (BRS) was measured by changes in HR and MAP after intravenous bolus injections of SNP and phenylephrine. Results: The vasodilatory effect of SNP significantly increased after SMF 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: Presented findings support the concept that the entire arterial system is under baroreflex control and that it is NO-dependent. The amplification of vascular smooth muscle cells sensitivity to NO suggested to be a new mechanism in baroreflex physiology, which can promote interactions between sympathetic nervous system and NO function, regenerating reduced NO bioavailability, a crucial mechanism of microvascular and endothelial dysfunction. These may generate important etiopathogenetic significance and potential therapeutic implementation in a spectrum of cardiovascular conditions, such as arterial hypertension, coronary heart disease, insulin resistance and diabetes, where sympathovagal imbalance exacerbated by derangements of NO signaling increases cardiovascular risk substantially.