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Heart 1998;80:127-133 ( August )
a Department of
Cardiovascular Medicine, University of Birmingham, Birmingham, UK, b Department of Physiology, University of
Birmingham
Correspondence to: Dr J C Vaile, Department of Cardiovascular Medicine, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, UK. email: j.c.vaile{at}bham.ac.uk
Accepted for publication 24 April 1998
Objective
To
investigate the effects of angiotensin II in the absence of baroreflex activation.
Design
Ten healthy
male volunteers were studied in a single blind, randomised, crossover
study of heart rate variability during intravenous angiotensin II
infusion (5-20 ng/kg/min) compared with a control pressor infusion of
phenylephrine (0.7-2.8 µg/kg/min). Each infusion was titrated to
increase mean blood pressure by 20 mm Hg; sodium nitroprusside was
then infused simultaneously to restore blood pressure to baseline values.
Results
During
concomitant angiotensin II (AII) and sodium nitroprusside (SNP)
infusion, the mean (SD) RR interval (864 (117) ms) was significantly
shorter than during phenylephrine (PE) and sodium nitroprusside
infusion (1057 (163) ms), and was significantly shorter than at
baseline (999 (164) ms), despite comparable levels of blood pressure.
Values of high frequency heart rate variability measured in the time
and frequency domains were significantly lower during AII/SNP infusion
than during PE/SNP: percentage of successive RR interval differences
exceeding 50 ms, 30(16)% v 57(21)%; root
mean square of successive RR interval differences, 63 (39)
v 90 (40) ms; high frequency power 0.48 (0.19) v 0.66 (0.26) nu.
Conclusions
When
the pressor response is controlled by sodium nitroprusside, angiotensin
II infusion is associated with tachycardia. Analysis of heart rate
variability suggests that this reflects inhibition of cardiac vagal activity.
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