Ambulatory Cardiovascular Activities in L-NAME-Treated Mice
Jong Y. Lee*, Silvia H. Azar
Identifiers and Pagination:Year: 2011
First Page: 23
Last Page: 32
Publisher Id: TOHYPERJ-4-23
Article History:Received Date: 16/06/2011
Revision Received Date: 21/08/2011
Acceptance Date: 12/09/2011
Electronic publication date: 04/11/2011
Collection year: 2011
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.