Short communicationEndomorphins decrease heart rate and blood pressure possibly by activating vagal afferents in anesthetized rats
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Acknowledgements
This study was supported by NIH Grants NS18710 and HL51314 from the Department of Health and Human Services.
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Vagal apnea and hypotension evoked by systemic injection of an antinociceptive analogue of endomorphin-2
2020, European Journal of PharmacologyCitation Excerpt :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.
Endomorphin-1 prevents lipid accumulation via CD36 down-regulation and modulates cytokines release from human lipid-laden macrophages
2011, PeptidesCitation Excerpt :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.
Neurochemical phenotypes of endomorphin-2-containing neurons in vagal nodose neurons of the adult rat
2009, Neurochemistry InternationalRespiratory and cardiovascular effects of biphalin in anaesthetized rats
2009, European Journal of PharmacologyCardiovascular responses to intravenous administration of human hemokinin-1 and its truncated form hemokinin-1(4-11) in anesthetized rats
2008, European Journal of PharmacologyEndomorphin 1 and endomorphin 2 suppress in vitro antibody formation at ultra-low concentrations: Anti-peptide antibodies but not opioid antagonists block the activity
2008, Brain, Behavior, and ImmunityCitation Excerpt :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).