title: Rostral ventrolateral medullary opioid receptor subtypes in the inhibitory effect of electroacupuncture on reflex autonomic response in cats.
abstract: Electroacupuncture (EA) is used in traditional Chinese medicine to treat arrhythmias, hypertension and myocardial ischemia. Our previous work suggests that the inhibitory effect of EA on the pressor reflex induced by bradykinin (BK) applied to the gallbladder is due, in part, to the activation of opioid receptors, most likely located in the rostral ventrolateral medulla (rVLM). However, specific opioid receptor subtypes, and hence the neurotransmitters. responsible for this inhibition are unknown. Therefore, in anesthetized cats, BK (10 microg/ml) was applied to the gallbladder to induce transient reflex increases in arterial blood pressure (BP). EA (1-2 mA, 5 Hz, 0.5 ms pulses) was delivered through acupuncture needles inserted bilaterally into Neiguan and Jianshi acupoints on forelimbs, overlying the median nerves. EA attenuated the BK-induced pressor response by 39%. Opioid receptor subtype antagonists or agonists were microinjected unilaterally into the rVLM. The mu- and delta-receptor antagonists CTOP and ICI 174,864, respectively, significantly attenuated the EA-induced inhibition for at least 30 min. The K-receptor antagonist (nor-BNI) was less effective and was shorter acting. Like EA, microinjection of mu- and delta-opioid agonists, DAGO and DADLE, respectively, into the rVLM significantly decreased the pressor responses. In contrast, the kappa-opioid agonist, U50,488, failed to alter the BK-induced pressor response. We conclude that a significant portion of inhibition of the gallbladder pressor response by EA is related to activation of mu- and delta-opioid receptors in the rVLM. The endogenous neurotransmitters for mu- and delta-opioid receptors, beta-endorphins and enkephalins, in the rVLM, therefore appear to play a role in the EA-related modulation of cardiovascular reflex responses. Conversely, dynorphin is less likely to be involved in this response.
authors.affiliation: Department of Medicine, College of Medicine, University of California, Irvine 92697-4075, USA.
authors.forename: P
authors.initials: P
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Tjen-A-Looi
authors.forename: J C
authors.initials: JC
authors.lastname: Longhurst
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology; D002415:Cats; D015671:Electroacupuncture; D004743:Enkephalin, Leucine / Q000031:analogs & derivatives* / Q000494:pharmacology; D016308:Enkephalin, Leucine-2-Alanine / Q000494:pharmacology; D005704:Gallbladder / Q000294:innervation / Q000502:physiology; D008526:Medulla Oblongata / Q000502:physiology*; D008845:Microinjections; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D011957:Receptors, Opioid / Q000502:physiology*; D017465:Receptors, Opioid, delta / Q000037:antagonists & inhibitors / Q000502:physiology; D017473:Receptors, Opioid, kappa / Q000037:antagonists & inhibitors / Q000502:physiology; D017450:Receptors, Opioid, mu / Q000037:antagonists & inhibitors / Q000502:physiology; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D013004:Somatostatin / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D017465:Receptors, Opioid, delta; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; C049352:phenylalanyl-cyclo(cysteinyltyrosyl-tryptophyl-ornithyl-threonyl-penicillamine)threoninamide; C051844:norbinaltorphimine; D013004:Somatostatin; D004743:Enkephalin, Leucine; D009271:Naltrexone; D016308:Enkephalin, Leucine-2-Alanine; C040643:N,N-diallyl-tyrosyl-alpha-aminoisobutyric acid-phenylalanyl-leucine