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Am J Physiol Heart Circ Physiol (June 26, 2009). doi:10.1152/ajpheart.00149.2009
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Submitted on February 12, 2009
Revised on June 22, 2009
Accepted on June 23, 2009

Spinal Nociceptin Mediates Electroacupuncture-Related Modulation of Visceral Sympathoexcitatory Reflex Response in Rats

Wei Zhou1*, Aman Mahajan1, and John C. Longhurst2

1 University of California, Los Angeles
2 University of California, Irvine

* To whom correspondence should be addressed. E-mail: WZhou{at}mednet.ucla.edu.

The role of nociceptin and its spinal cord neural pathways in electroacupuncture (EA)-related inhibition of visceral excitatory reflexes is not clear. Nociceptin/orphanin FQ (N/OFQ) is an endogenous ligand for a G-protein coupled receptor, called the N/OFQ peptide (NOP) receptor, which has been found to be distributed in the spinal cord. The present study investigated the importance of this system in visceral-cardiovascular reflex modulation during EA. Cardiovascular pressor reflex responses were induced by gastric distension in Sprague-Dawley rats anesthetized by ketamine and xylazine. Intrathecal injection of nociceptin (10 nM) at T1-2 attenuated the pressor responses by 35%, similar to the influence of EA at P 5-6 (42% decrease). Intrathecal injection of the NOP antagonist, [N-Phe1]-nociceptin (1-13) NH2 partially reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not alter the EA-like inhibitory effect of nociceptin on the pressor reflex, while a combination of nociceptin receptor antagonist with naloxone completely abolished the EA response. Intrathecal injection of nociceptin attenuated the pressor responses to electrical stimulation of the rostral ventrolateral medulla by 46% suggesting that nociceptin can regulate sympathetic outflow. Furthermore, bilateral microinjection of NOP antagonist into either the dorsal horn or the intermediolateral column at T1 partially reversed the EA inhibitory effect. These results suggest that nociceptin in the spinal cord mediates part of the EA-related modulation of visceral reflex responses.







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