Leucine-enkephalin increases the level of inositol (1,4,5) triphosphate and releases calcium from an intracellular pool in rat ventricular cardiac myocytes.

C. Ventura, E. G. Lakatta, A. Sisini, M. P. Campus, M. C. Capogrossi

Research output: Contribution to journalArticlepeer-review

Abstract

In rat ventricular cardiomyocytes loaded with the fluorescent Ca2+ indicator Indo-1/AM, the delta opioid receptor agonist Leu-Enk caused Cai oscillations and abolished the caffeine-induced Cai transient. During superfusion of cardiomyocytes with the specific opioid antagonist naloxone, Cai is not affected by Leu-Enk and the caffeine-triggered Cai transient is preserved. In parallel experiments with cardiac myocytes, the delta opioid agonist increased the intracellular level of Ins (1,4,5) P3 by about 4 times above the control value. Such an effect was completely antagonized by naloxone. Thus, Leu-Enk induces depletion of Ca2+ from the SR by a receptor-mediated mechanism which appears to involve an increase in the intracellular level of Ins (1,4,5) P3.

Original languageEnglish
Pages (from-to)261-266
Number of pages6
JournalBollettino della Societa Italiana di Biologia Sperimentale
Volume67
Issue number3
Publication statusPublished - Mar 1991

ASJC Scopus subject areas

  • Medicine(all)

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