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1 Dept. of Integrative Physiology, The University of Iowa, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: harald-stauss{at}uiowa.edu.
The mechanisms generating high frequency (HF) and low frequency (LF) blood pressure variability (BPV) are reasonably well understood. However, little is known about the origin of very low frequency (VLF) BPV. We tested the hypothesis that VLF BPV is generated by L-type Ca++-channel-dependent mechanisms. In conscious rats, arterial blood pressure was recorded during control conditions (n=8) and ganglionic blockade (n=7), while increasing doses (0.01-5.0 mg/100µL/h) of the L-type Ca++-channel blocker nifedipine were infused intravenously. VLF (0.02-0.2 Hz), LF (0.2-0.6 Hz), and HF (0.6-3.0 Hz) BPV were assessed by spectral analysis of systolic blood pressure. During control conditions, nifedipine caused dose-dependent declines in VLF and LF BPV, while HF BPV was not affected. At the highest dose of nifedipine VLF BPV was reduced by 86% compared to baseline, indicating that VLF BPV is largely mediated by L-type Ca++-channel-dependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca++-channels than LF BPV, because lower doses of nifedipine were required to significantly reduce VLF BPV than to reduce LF BPV. Ganglionic blockade markedly reduced VLF and LF BPV and abolished the nifedipine-induced dose-dependent declines in VLF and LF BPV, suggesting that VLF and LF BPV require sympathetic activity to be evident. In conclusion, VLF BPV is largely mediated by L-type Ca++-channel-dependent mechanisms. We speculate that VLF BPV is generated by myogenic vascular responses to spontaneously occurring perturbations of blood pressure. Other factors, such as sympathetic nervous system activity may elicit a permissive effect on VLF BPV by increasing vascular myogenic responsiveness.
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