Langager AM, Hammerberg BE, Rotella DL, Stauss HM. Very low-frequency blood pressure variability depends on voltage-gated L-type Ca 2ϩ channels in conscious rats. Am J Physiol Heart Circ Physiol 292: H1321-H1327, 2007. First published October 20, 2006; doi:10.1152/ajpheart.00874.2006.-The mechanisms generating highfrequency (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 2ϩ channel-dependent mechanisms. In conscious rats, arterial blood pressure was recorded during control conditions (n ϭ 8) and ganglionic blockade (n ϭ 7) while increasing doses (0.01-5.0 mg ⅐ 100 l Ϫ1 ⅐ h Ϫ1 ) of the L-type Ca 2ϩ 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 Ca 2ϩ channeldependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca 2ϩ 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 2ϩ 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 BLOOD PRESSURE VARIABILITY has received considerable attention during the last decades, not only because enhanced blood pressure variability has been identified as an independent cardiovascular risk factor (33, 35) but also because the patterns of blood pressure variability may provide important insights into cardiovascular regulation (2, 23, 31). Highfrequency (HF) blood pressure variability linked to respiration has been suggested to involve fluctuations in cardiac output of purely mechanical origin (23), secondary to respiratory sinus arrhythmia (2). Low-frequency (LF) blood pressure fluctuations (0.2-0.6 Hz in rats), the so-called Mayer waves (36), have been associated mostly with sympathetic modulation of vascular tone (22, 50, 52). However, very low-frequency (VLF) blood pressure fluctuations (0.02-0.2 Hz in rats) at frequencies below the frequency of Mayer waves are less well understood. A variety of facto...