Modulation of cardiovascular excitatory responses in rats by transcutaneous magnetic stimulation: role of the spinal cord

Abstract

This study investigated the efficacy of magnetic stimulation on the reflex cardiovascular responses induced by gastric distension in anesthetized rats and compared these responses to those influenced by electroacupuncture (EA). Unilateral magnetic stimulation (30% intensity, 2 Hz) at the Jianshi-Neiguan acupoints (pericardial meridian, P 5–6) overlying the median nerve on the forelimb for 24 min significantly decreased the reflex pressor response by 32%. This effect was noticeable by 20 min of magnetic stimulation and continued for 24 min. Median nerve denervation abolished the inhibitory effect of magnetic stimulation, indicating the importance of somatic afferent input. Unilateral EA (0.3–0.5 mA, 2 Hz) at P 5–6 using similar durations of stimulation similarly inhibited the response (35%). The inhibitory effects of EA occurred earlier and were marginally longer (20 min) than magnetic stimulation. Magnetic stimulation at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37–39) overlying the superficial peroneal nerve on the hindlimb did not attenuate the reflex. Intravenous naloxone immediately after termination of magnetic stimulation reversed inhibition of the cardiovascular reflex, suggesting involvement of the opioid system. Also, intrathecal injection of δ- and κ-opioid receptors antagonists, ICI174,864 ( n = 7) and nor-binaltorphimine ( n = 6) immediately after termination of magnetic stimulation reversed inhibition of the cardiovascular reflex. In contrast, the μ-opioid antagonist CTOP ( n = 7) failed to alter the cardiovascular reflex. The endogenous neurotransmitters for δ- and κ-opioid receptors, enkephalins and dynorphin but not β-endorphin, therefore appear to play significant roles in the spinal cord in mediating magnetic stimulation-induced modulation of cardiovascular reflex responses.