Abstract

We have shown that the hypothalamic ARC sends excitatory projections to midbrain vlPAG, and vlPAG is essential to the inhibitory effect of EA on the reflex increase in blood pressure (BP) and rostral ventrolateral medulla (rVLM) neuronal reflex response. The present study evaluated for possible inhibition of rVLM neurons by EA through excitation of ARC and vlPAG. In α-chloralose anesthetized cats, stimulation electrodes were placed around the SN and acupuncture needles were inserted at P5–6, located over the median nerve. Electrophysiological recordings showed that ARC and vlPAG neurons received convergent afferent input from SN and somatic acupoints. EA at P5–6 for 30 min excited both ARC and vlPAG neurons and inhibited rVLM neurons. Microinjection of the excitatory amino acid, D, L-homocysteic acid (DLH 4 nM, 50 nl) into ARC (n=14) like EA augmented the responses of vlPAG neurons and inhibited the rVLM neuronal response to SN stimulation (n=6). The inhibition of rVLM neurons by EA and microinjection of DLH into ARC were each blocked by microinjection of kainic acid (KA 1 mM, 50 nl) into the vlPAG (n=6). Hemodynamic study also showed that EA or microinjection of DLH bilaterally into ARC (n=5) inhibited the visceral stimulation-induced pressor reflex for 5–20 min. However, when KA was microinjected into the vlPAG, this inhibition was blocked (n=7). These results suggest that ARC neurons excited by EA send excitatory projections to the vlPAG, which, in turn, provided inhibitory projections to the rVLM to modulate the increase in BP during visceral afferent stimulation. (Supported by NIH HL-72125 and HL-63313).

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