Methods Blood pressure variability was evaluated in conscious Wistar contro
l rats and rats with established L-NAME hypertension (20 mg/kg pr 24 h, 4 w
eeks).
Results Final systolic arterial pressure was 185 +/- 5 and 132 +/- 4 mmHg i
n the N-omega-nitro-L-arginine methyl ester (L-NAME)-treated and control ra
ts, respectively, The standard deviation of systolic arterial pressure in t
he L-NAME group was 70% greater than in the control rats, indicating a sign
ificant increase in the overall variability. Arterial pressure in the L-NAM
E rats exhibited aperiodical, abrupt rises and falls and data was grossly n
on-stationary. Blood pressure variability was therefore evaluated using Poi
ncare plot analysis. The variance of the difference (delta) between two suc
cessive values of systolic arterial pressure, determined for time intervals
of 0.2 to 5 s (0.2 s increment), was always significantly higher in the L-
NAME group compared with untreated animals. The variance of delta systolic
arterial pressure increased with the time interval and plateaued for time i
ntervals of 2.4 and 1.4 s in hypertensive and normotensive rats, respective
ly. These differences vanished when the sudden events observed in L-NAME ra
ts were omitted in the construction of Poincare plots. Acute administration
of prazosin (1 mg/kg), but not losartan (10 mg/kg) markedly reduced the va
riance of delta systolic arterial pressure in hypertensive rats.
Conclusions Nitric oxide participates in the control of arterial pressure v
ariability. The sympathetic nervous system seems to be a major determinant
of the increased short-term variability of arterial pressure in this model.
(C) Lippincott Williams & Wilkins.