Elsevier

Brain Research

Volume 803, Issues 1–2, 24 August 1998, Pages 204-207
Brain Research

Short communication
Endomorphins decrease heart rate and blood pressure possibly by activating vagal afferents in anesthetized rats

https://doi.org/10.1016/S0006-8993(98)00623-4Get rights and content

Abstract

Endomorphin 1 (10, 30, 100 nmol/kg) administered intravenously (i.v.) to urethane-anesthetized rats consistently and dose-dependently lowered heart rate (HR) and mean arterial pressure (MAP); the decrease in blood pressure recovered faster as compared to the HR. The effects of endomorphin 2 were qualitatively similar. Naloxone (2 mg/kg, i.v.) completely antagonized the bradycardia and hypotension caused by endomorphin 1. Pretreatment of the rats with atropine methylnitrate, atropine sulfate (2 mg/kg, i.v.) or bilateral vagotomy nearly abolished the bradycardia and attenuated the hypotensive effect of endomorphin 1. Our studies suggest that the bradycardia effect following systemic administration of the new opioid peptide may be explained by activation of vagal afferents and the hypotensive effect may be secondary to a reduction of cardiac output and/or a direct vasodilation.

Section snippets

Acknowledgements

This study was supported by NIH Grants NS18710 and HL51314 from the Department of Health and Human Services.

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    This shows that excitation of μ opioid receptors expressed on vagi nerves is responsible for the generation of the responses. It is consistent with the results of a previously reported study by Kwok and Dun (1998). These authors suggested the existence of dependence between heart rate decrease as well as hypotension evoked by EM-1 and the activation of vagal afferents.

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    These substances bind to and activate several opioid receptors, among which the four major subtypes are the three classical MOP, DOP and KOP receptors and the non classical (nociceptin) NOP receptor [26,6]. Through the action of the three classical receptors, but above all of MOP, EM-1 is known to induce hypotension [10], influence appetite [25], impair spatial learning [27] and cause analgesia [19], as well as bearing rewarding and addictive properties [24]. Furthermore, it has been recently reported that EM-1 can cross the blood-brain barrier [13], thus entering the blood flow and possibly reaching several peripheral body districts, where its concentrations vary from 10−12 to 10−6 M. Coherently, EM-1 has been identified in the rat spleen and thymus as well as in spleens from human patients [20], thus having the physiological potential to influence immunological function through opioid receptors.

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    At the cellular level, EMs have been found to activate G proteins (Alt et al., 1998; Sim et al., 1998; Harrison et al., 1998; Monory et al., 2000), regulate different types of adenylyl cyclase isoenzymes (Nevo et al., 2000), inhibit membrane-calcium currents (Mima et al., 1997; Higashida et al., 1998), activate inward K+ currents (Gong et al., 1998), and modulate the differential expression of MOR mRNA and MOR function in SHSY-5Y cells (Yu et al., 2003). Moreover, these peptides display many physiological activities normally attributed to opiate alkaloids, such as pain modulation (Przewlocka et al., 1999; Przewlocki et al., 1999; Ohsawa et al., 2001; Zadina,2002), feeding responses (Asakawa et al., 1998), oxygen consumption (Asakawa et al., 2000), vasodepressor and cardiorespiratory regulation (Champion et al., 1997; Kwok and Dun,1998; Czapala et al., 2000), neuroendocrine modulation (Coventry et al., 2001; Doi et al., 2001), learning and memory behavioral responses (Ukai et al., 2001), and immune regulation (Azuma and Ohura, 2002b). EMs have been shown to be present in cells and tissues of the immune system (Jessop et al., 2000, 2002; Mousa et al., 2002; Seale et al., 2004), and to alter a variety of immune parameters (Azuma et al., 2000, 2002; Azuma and Ohura, 2002a,b).

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