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High blood pressure (BP) is a dominant risk factor in cardiovascular diseases. An experimental
model of nitric oxide synthase (NOS) inhibitor induced hypertension was developed to study some etiologic mechanisms
in cardiovascular parameters.
Cardiovascular rhythm characteristics were documented in mice following the N-omega-nitro-L-argininemethyl-
ester (L-NAME)-treatment (Rx). Radio-telemetered BP, heart rate (HR), and locomotor activity (LA) were
measured every 4 min for 5 days before and for 14 days after Rx. Data was converted into an hourly average and analyzed
by the linear least square rhythmometry.
L-NAME-Rx increased systolic BP (SBP) significantly without significant changes in diastolic BP and markedly
reduced HR: SBP (mm Hg) 143.4 ± 0.6 versus 148.9 ± 0.4, P <0.0001; HR (beat/min): 552.13 ± 2.7 vs. 481 ± 1.8, P
<0.0001, with markedly depleted amplitude. SBP variations were mainly during the night time, while HR variations were
almost every time-point comparison throughout the 24-h span. Although the overall LA was not significantly changed
with L-NAME-Rx, time-point depleted LA was noted, especially when the light was off at 18:00 hour through midnight
(P <0.0001), while an opposite result was observed at noon with significantly increased LA in this nocturnal animal (P
<0.005), with markedly decreased amplitude (P <0.01). Interestingly, we observe reduced HR with L-NAME-Rx
contradicted to other reports.
The results suggest that the NOS blockade may impair cardiovascular autonomic adaptations and arterial
baroreflex integration, resulting in an increased vascular tone during the systole, but not an end diastole in the relaxed
cardiac autonomic tonus.