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<jats:p> Nitric oxide (NO) donors inhibit sympathetic neurotransmission and baroreceptor activity and can directly stimulate heart rate (HR) in vitro. To assess whether exogenous NO affects cardiovascular autonomic control in humans, we tested the baroreceptor-cardiac reflex [baroreflex sensitivity (BRS)] and the arterial blood pressure (BP) and HR variability during an infusion of the NO donor sodium nitroprusside (SNP, 2 μg ⋅ kg<jats:sup>−1</jats:sup> ⋅ min<jats:sup>−1</jats:sup>) or 5% glucose in 16 healthy subjects. The hypotensive action of SNP was prevented by phenylephrine (PE, 0.9 ± 0.15 μg ⋅ kg<jats:sup>−1</jats:sup> ⋅ min<jats:sup>−1</jats:sup>). The SNP + PE infusion did not affect BRS or HR variability, but it caused a significant reduction in the diastolic and systolic BP low-frequency power. In addition, SNP + PE caused a sustained 12% increase in HR in the absence of changes in brachial and aortic BP. In conclusion, SNP had no effect on the cardiac-vagal limb of the baroreflex in humans but caused a substantial reduction in BP low-frequency power consistent with a decreased baroreflex/sympathetic control of peripheral resistance. The increase in HR in the absence of baroreceptor downloading confirms our previous finding of a direct positive chronotropic effect of NO donors. </jats:p>

Original publication




Journal article


American Journal of Physiology-Heart and Circulatory Physiology


American Physiological Society

Publication Date





H221 - H227