Effect of exogenous nitric oxide on baroreflex function in humans

Citation
N. Hogan et al., Effect of exogenous nitric oxide on baroreflex function in humans, AM J P-HEAR, 46(1), 1999, pp. H221-H227
Citations number
42
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
46
Issue
1
Year of publication
1999
Pages
H221 - H227
Database
ISI
SICI code
0363-6135(199907)46:1<H221:EOENOO>2.0.ZU;2-E
Abstract
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.