(Hypertension. 2000;36:264.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Departments of Cardiovascular Medicine (S.C., J.C.V., J.N.T.) and Physiology (J.F., H.F.R., J.H.C.), University of Birmingham, UK.
Correspondence to Dr S. Chowdhary, Department of Cardiovascular Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, UK. E-mail S.Chowdhary{at}bham.ac.uk
AbstractCardiac
autonomic control is of prognostic significance in cardiac disease, yet
the control mechanisms of this system remain poorly defined. Animal
data suggest that nitric oxide (NO) modulates cardiac autonomic
control. We investigated the influence of NO on the baroreflex control
of heart rate in healthy human subjects. In 26 healthy male volunteers
(mean age, 23±5 years), we measured heart rate variability and
baroreflex sensitivity during inhibition of endogenous NO
production with
NG-monomethyl-L-arginine
(L-NMMA) (3 mg/kg per hour) and during exogenous NO donation with
sodium nitroprusside (1 to 3 mg/h). Increases from baseline (
) in
high-frequency (HF) indexes of heart rate variability were smaller with
L-NMMA in comparison to an equipressor dose of the control
vasoconstrictor phenylephrine (12 to 42 µg/kg per hour):
root mean square of successive RR interval differences
(
RMSSD)=23±32 versus 51±48 ms (P<0.002);
percentage of successive RR interval differences >50 ms
(
pNN50)=5±15% versus 14±12% (P<0.05); and
HF
normalized power=-2±7 versus 9±8 normalized units
(P<0.01), respectively. Relative preservation of these
indexes was observed during unloading of the baroreflex with sodium
nitroprusside compared with a matched fall in blood pressure produced
by a control vasodilator, hydralazine (9 to 18 mg/h):
RMSSD=-8±8 versus -24±15 ms (P<0.001);
pNN50=-6±11% versus -15±19% (P<0.01);
HF
normalized power=-7±13 versus -13±11 normalized units
(P<0.05), respectively. The change in cross-spectral
-index calculated as the square root of the ratio of RR interval
power to systolic spectral power in the HF band (although not
-index calculated in the same way for the low-frequency bands or
baroreflex sensitivity assessed by the phenylephrine bolus
method) was attenuated with L-NMMA compared with
phenylephrine (
=4±8 versus 14±15 ms/mm Hg,
respectively; P<0.02) and with sodium nitroprusside
compared with hydralazine (
=-7±6 and -9±7 ms/mm Hg,
respectively; P<0.05). In conclusion, these data
demonstrate that NO augments cardiac vagal control in humans.
Key Words: nitric oxide heart rate baroreceptors autonomic nervous system blood pressure
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