抄録
It is well known that the low-frequency oscillations (<0.6 Hz) in blood pressure reflect sympathetic activity to the resistance vessels and that the nitric oxide (NO) system is a potent mechanism in buffering these blood pressure oscillations of central origin. In the present study, the buffering effect of NO on sympathetic activity was investigated by power spectral analysis of arterial pressure in conscious normotensive rats. Ganglion blocker hexamethonium bromide (C6), Nω-nitro-L-arginine methyl ester (L-NAME), and L-arginine (L-Arg) were used to examine the hemodynamic effects of the NO system and the sympathetic nervous system on mean arterial pressure (MAP), mean heart rate (MHR), arterial pressure variability (APV) and heart rate variability (HRV). APV (<0.25 Hz) increased with the significant increase of MAP after administration of L-NAME, while APV (0.25~0.6 Hz) decreased. In addition, elevated APV (<0.25 Hz) decreased with the significant decrease of MAP by addition of L-Arg, while APV (0.25~0.6 Hz) increased. Oscillations <0.6 Hz of APV were eliminated by C6 and C6 + prazosin (α1-blocker) and MAP decreased by 20 mmHg. MHR decreased by L-NAME and increased by L-Arg. HRV (<0.6 Hz) reflected sympathetic activity to the heart. These results suggest that, (1) APV (<0.6 Hz) is originated from the sympathetic nervous system, (2) the buffering effect of NO on APV is below 0.6 Hz and the effect of NO on APV (0.25~0.6 Hz) is exerted via baroreflex, and (3) NO interacts with sympathetic activity by reducing the Ca2+ concentration in smooth muscle cells. [Jpn J Physiol 54 Suppl:S97 (2004)]
