title: Endomorphin-2 in the medial NTS attenuates the responses to baroreflex activation.
abstract: We have previously reported that microinjections of endomorphin-2 (E-2; an endogenous mu-receptor agonist) into the medial subnucleus of the NTS (mNTS) elicit depressor and bradycardic responses via activation of ionotropic glutamate receptors located on secondary mNTS-neurons. Based on this report, it was hypothesized that activation of secondary mNTS neurons by E-2 may result in an exaggeration of baroreflex responses. In order to test this hypothesis, baroreflex responses were studied in adult, urethane-anesthetized, artificially ventilated, male Wistar rats before and after the microinjections of E-2 into the mNTS. Baroreceptors were stimulated by applying pressure increments (80-100 mm Hg) in the carotid sinus and by electrical stimulation (stimulus intensity: 0.5 V, frequencies 5, 10, and 25 pulses/s, pulse duration: 1 ms) of the aortic nerve for 30-s periods. Baroreceptor stimulation elicited depressor and bradycardic responses. Microinjections (100 nl) of E-2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses. Microinjections of naloxone (an opioid receptor antagonist) into the mNTS (0.5 mmol/l) did not alter baroreflex responses. Based on these results, it was concluded that activation of mu-opioid receptors in the mNTS attenuates baroreflex responses. Possible mechanisms for excitatory effects of E-2 in the mNTS resulting in depressor and bradycardic responses, on one hand, and inhibitory effects resulting in attenuation of baroreflex responses, on the other, are discussed.
authors.affiliation: Department of Neurological Surgery, MSB H-586, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103, USA.
authors.forename: Eddy
authors.initials: E
authors.lastname: Viard
authors.forename: Hreday N
authors.initials: HN
authors.lastname: Sapru
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D017704:Baroreflex / Q000187:drug effects* / Q000528:radiation effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D002346:Carotid Sinus / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D004558:Electric Stimulation / Q000379:methods; D018698:Glutamic Acid / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008297:Male; D008845:Microinjections / Q000379:methods; D008959:Models, Neurological; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009842:Oligopeptides / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D017552:Solitary Nucleus / Q000187:drug effects*; D013997:Time Factors; D014630:Vagus Nerve / Q000187:drug effects / Q000528:radiation effects
chemical_list: D000701:Analgesics, Opioid; D009292:Narcotic Antagonists; D009842:Oligopeptides; D009270:Naloxone; D018698:Glutamic Acid; C105294:endomorphin 2