Submitted on December 6, 2004
Accepted on June 3, 2005
Frequency-dependent Baroreflex Modulation of Blood Pressure and Heart Rate Variability in Conscious Mice
Rubens Fazan Jr1*, Mauro Oliveira1, Valdo Jose Dias da Silva2, Luis F Joaquim1, Nicola Montano3, Alberto Porta3, Mark W Chapleau4, and Helio C Salgado1
1 Department of Physiology, School of Medicine of Ribeirao Preto, USP, Ribeirao Preto, SP, Brazil
2 Department of Biological Sciences, School of Medicine of Triangulo Mineiro, Uberaba, MG, Brazil
3 Dipartimento di Scienze Cliniche, Medicina Interna II, Universita degli Studi di Milano, Milano, Italy
4 Deaprtments of Internal Medicine and Physiology & Biophysics, University of Iowa, and Veterans Affairs Medicial Center, Iowa City, Iowa, USA
* To whom correspondence should be addressed. E-mail: rfazanjr{at}rfi.fmrp.usp.br.
The baroreceptor reflex buffers fluctuations in arterial pressure (AP), in part by eliciting reflex changes in heart rate (HR). The goal of this study was to determine the baroreflex influence on total, low frequency (LF), and high frequency (HF) systolic AP and pulse interval (PI) variability in conscious mice. Systolic AP and PI were measured in C57Bl/6J mice previously subjected to sinoaortic baroreceptor deafferentation (SAD, n=21) or sham surgery (n=20). Average systolic AP and PI did not differ in SAD and control mice. In contrast, systolic AP variance was markedly enhanced (21±4 vs. 9.5±1 mmHg2) and PI variance significantly reduced (8.8±2 vs. 26±6 ms2) in SAD vs. control mice, respectively. HF (1-5 Hz) systolic AP variability quantified by spectral analysis was significantly greater in SAD (8.5±2.0 mmHg2) compared with control (2.5±0.2 mmHg2) mice, while LF (0.1-1 Hz) systolic AP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5±0.1 vs. 10.8±3.4 ms2) while HF PI variability did not differ. LF oscillations in systolic AP and PI were coherent in control mice (coherence = 0.68±0.05) with changes in systolic AP leading changes in PI (phase = -1.41±0.06 radians), but were not coherent in SAD mice (coherence = 0.08±0.03). Blockade of parasympathetic control of heart rate with atropine decreased average PI, PI variance, and LF and HF PI variability in control mice (n=10), but had no effect on these variables in SAD mice (n=6). In control mice, blockade of sympathetic control of heart rate with propranolol increased average PI and decreased PI variance and LF PI variability (n=6). In SAD mice, propranolol increased average PI but did not influence PI variability (n=6). We conclude: 1) Baroreflex modulation of PI contributes to LF, but not HF PI variability and is mediated by both sympathetic and parasympathetic nervous systems in conscious mice; and 2) The baroreflex limits HF of systolic AP variability despite the lack of baroreflex control of PI in this frequency range.
