Role of μ-opioid receptors in insulin release in the presence of inhibitory and excitatory secretagogues
Autor: | María Carmen Iglesias-Osma, Julio Moratinos, Raquel E. Rodríguez, María José García-Barrado, Mariano Martín |
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Rok vydání: | 2002 |
Předmět: |
medicine.medical_specialty
Carbachol medicine.drug_class Receptors Opioid mu (+)-Naloxone Biology Clonidine Glibenclamide Islets of Langerhans Mice chemistry.chemical_compound Quinoxalines Internal medicine Glyburide Insulin Secretion Adrenergic alpha-2 Receptor Agonists medicine Animals Insulin Drug Interactions Endogenous opioid Pharmacology Forskolin Naloxone Pancreatic islets Receptor antagonist Endocrinology medicine.anatomical_structure Opioid chemistry Brimonidine Tartrate Female Somatostatin medicine.drug |
Zdroj: | European Journal of Pharmacology. 448:95-104 |
ISSN: | 0014-2999 |
DOI: | 10.1016/s0014-2999(02)01897-6 |
Popis: | In mouse pancreatic islets incubated under static conditions, the inhibitory effects on glucose-evoked insulin release induced by adrenaline (1 microM), clonidine (2 microM) and UK 14,304 (brimonidine, 0.001-1 microM) were abolished by naloxone (30 nM). Only CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH(2), 0.1 microM), a very selective mu-opioid receptor antagonist, blocked the response to UK 14,304. Glucose-induced insulin secretion was attenuated by both beta-endorphin (0.01 microM) and endomorphin-1 (0.1 microM). Naloxone and CTOP prevented these inhibitory responses. The stimulatory effect of glibenclamide (1 microM) was also reduced by endomorphin-1. However, when islets were incubated in the presence of K(+) (30 mM), carbachol (100 microM) or forskolin (0.1 microM), neither the inhibitory effect induced by UK 14,304 was reversed by naloxone, nor endomorphin-1 altered the responses promoted by the excitatory agents. Thus, alpha(2)-adrenoceptor stimulation might inhibit glucose-induced insulin secretion by releasing endogenous opioids. Mu-Opioid receptor activation and opening of K(ATP) channels could be involved in the response. |
Databáze: | OpenAIRE |
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