Nitric oxide (NO) donors inhibit sympathetic neurotransmission and barorece
ptor activity and can directly stimulate heart rate (HR) in vitro. To asses
s whether exogenous NO affects cardiovascular autonomic control in humans,
we tested the baroreceptor-cardiac reflex [baroreflex sensitivity (BRS)I an
d the arterial blood pressure (BP) and HR variability during an infusion of
the NO donor sodium nitroprusside (SNP, 2 mu g . kg(-1) . min(-1)) or 5% g
lucose in 16 healthy subjects. The hypotensive action of SNP was prevented
by phenylephrine (PE, 0.9 +/- 0.15 mu g . kg(-1) . min(-1)). The SNP + PE i
nfusion did not affect BRS or HR variability, but it caused a significant r
eduction 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 i
n brachial and aortic BP. In conclusion, SNP had no effect on the cardiac-v
agal 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 baro
receptor downloading confirms our previous finding of a direct positive chr
onotropic effect of NO donors.