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This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/H1321    most recent 00874.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Langager, A. M. Articles by Stauss, H. M. Search for Related Content PubMed PubMed Citation Articles by Langager, A. M. Articles by Stauss, H. M.

Very low-frequency blood pressure variability depends on voltage-gated L-type Ca²⁺ channels in conscious rats

Department of Integrative Physiology, The University of Iowa, Iowa City, Iowa

Submitted 14 August 2006 ; accepted in final form 13 October 2006

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 Ca²⁺ 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·100 µl^–1·h^–1) of the L-type Ca²⁺ 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, whereas HF BPV was not affected. At the highest dose of nifedipine, VLF BPV was reduced by 86% compared with baseline, indicating that VLF BPV is largely mediated by L-type Ca²⁺ channel-dependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca²⁺ 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 Ca²⁺ 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.

power spectral analysis; myogenic vascular function; nifedipine; autonomic nervous system; ganglionic blockade

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