Abstract
The objectives of this study were to determine the effects of L-arginine-derived nitric oxide (NO) synthesis and noradrenergic function on skin electrical resistance of acupoints and meridians. Experiments were performed on male Sprague-Dawley rats anesthetized with sodium pentobarbital. Low skin-resistance points (LSRP; BL 56, PC 6, CV 17), non-LSRP positions (along the meridians), and non- LSRP, non-meridian control positions (adjacent to but not along the meridians) were determined on the skin surface by measurements of the skin stimulus-evoked electrical currents. The effects of L-arginine-derived NO synthesis and noradrenergic function on the currents, representing skin electrical resistance, were examined in the LSRP, non-LSRP, and non-meridian control points. The skin stimulus-evoked electrical currents at BL 56 (36.4 +/- 1.4 microA), PC 6 (35.4 +/- 1.2), and CV 17 (33.1 +/- 1.4) were significantly higher than those in non-LSRP and non-meridian control positions (p < 0.01, n = 7). The currents were consistently increased after repeated stimulation along the skin as a function of time. Intravenous injections of L-arginine (3 mg/kg, 10 mg/kg, and 30 mg/kg) and 3-morpholinyl-sydnoneimine (SIN-1; 1 microg/kg, 3 microg/kg, and 10 microg/kg) produced dose-dependent increases in the currents (p < 0.05, n = 5-6), but currents were not altered by injections of D-arginine (3 mg/kg, 10 mg/kg, and 30 mg/kg). Stimulus-evoked increases in currents were blocked by intravenous injections of either N (G)-propyl-L-arginine (NPLA, 3 mg/kg), N-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg), or guanethidine (3 mg/kg), a noradrenergic blockade. This is the first evidence showing that L-arginine-derived NO synthesis and noradrenergic transmission modify the skin electric conductance of LSRP. L-Arginine-derived NO synthesis appears to mediate noradrenergic function on skin sympathetic nerve activation, which contributes to low resistance characteristics of acupoints and meridians.
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