抄録
We previously reported that low-frequency variability (< 0.6 Hz) in arterial pressure (AP) oscillations originates from sympathetic activity and is buffered by nitric oxide (NO). The power spectral density (PSD) in the 0–0.2 Hz (VLF) band was increased by L-NAME, while the PSD in the 0.2–0.6 Hz (LF) band was decreased. In contrast, L-Arg decreased the PSD in the VLF band and increased the PSD in the LF band. This shows that NO buffers low-frequency variability of AP oscillations via two-pathways. In the present study, we investigated the mechanical pathways of NO-buffering action on AP variability to assess the role of NO in blood pressure regulation. We conducted experiments on male normotensive Wistar rats (n = 30), 10–13 wks of age in order to examine the dynamic effects of NO and KATP channels on AP variability and heart rate variability (measured in the conscious resting state). Findings indicate that (1) the PSD in the VLF band increases with the increase in mean AP by the NO-buffering mechanism at resistance vessels, and (2) the PSD in the LF band decreases with the increase in mean AP by the NO-buffering mechanism via the baroreflex, which is complemented by activating KATP channels of baroreceptors. We conclude that VLF variability is a risk factor exerting serious damage on the cardiovascular system during an increase in AP, while LF variability is a homeostatic control factor maintaining the fluctuation of AP within a narrow range via the baroreflex. [J Physiol Sci. 2007;57 Suppl:S210]
