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Dynorphin gene expression and release in the myocardial cell.

1994; Elsevier BV; Volume: 269; Issue: 7 Linguagem: Inglês

10.1016/s0021-9258(17)37698-6

1083-351X

Carlo Ventura, Carlo Guarnieri, Isabella Vaona, Gabriele Campana, Gianfranco Pintus, Santi Spampinato,

Neurotransmitter Receptor Influence on Behavior

The expression of the prodynorphin gene was investigated in adult cultured rat ventricular cardiac myocytes by using a sensitive solution hybridization RNase protection assay for the quantitative analysis of prodynorphin mRNA.Myocyte culture in high KC1 resulted, after 4 h, in a marked increase in cellular prodynorphin mRNA, while a KC1 treatment for 6, 12, or 24 h progressively down-regulated the levels of prodynorphin mRNA below the control value.Immunoreactive dynorphin B, a biologically active end product of the precursor, was found to be present in the culture medium in significantly higher amounts than in the cardiac myocytes.The levels of this biologically active K opioid receptor agonist significantly increased after 4 h of KC1 treatment and were markedly reduced following a 24-h exposure of the cardiac myocytes to KCl.These KC1-induced effects were all abolished by cell incubation in the presence of the calcium channel blocker verapamil.In single cardiac myocytes, acute stimulation of K opioid receptors with dynorphin B or with the selective agonist U-50,488H increased the level of cytosolic calcium.This effect was abolished by the specific K opioid receptor antagonist (Mr-1452) and was not affected by the removal of calcium from the bathing medium.These results suggest that an opioid gene may influence the myocardial function in an autocrine or paracrine fashion.