Beta-adrenergic regulation of gap-junctional intercellular communication in cultured rabbit gastric epithelial cells.

The effect of a beta-adrenergic agonist, isoproterenol, on gap-junctional intercellular communication (GJIC) and intracellular cyclic AMP (cAMP) content was investigated in cultured rabbit gastric epithelial cells. Isoproterenol rapidly enhanced GJIC determined by the Lucifer yellow transfer at 10(-6) and 10(-5) M but the effect at 10(-6) M was variable. The enhancement of GJIC by 10(-5) M isoproterenol, which disappeared within 10 or 30 min, was inhibited by a beta blocker, propranolol. Isoproterenol (10(-6) M) greatly increased cAMP at 5 min and much more so at 20 min after its addition. Colforsin (also known as forskolin) and 3-isobutyl-1-methylxanthine (IBMX) enhanced GJIC until 16 and 20 min after their addition, respectively. Both colforsin and IBMX increased the cAMP content by a lesser extent than 10(-6) M isoproterenol. Isoproterenol (10(-5) M) inhibited the GJIC enhanced by colforsin or IBMX. Propranolol abolished the inhibition of GJIC by isoproterenol in the presence of IBMX. Both amiloride, an inhibitor of the Na+/H+ exchanger, and nigericin, a K+/H+ antiporter, inhibited the GJIC enhanced by isoproterenol, IBMX, colforsin and irsogladine. An inhibitor of cAMP-dependent protein kinase A, H-89 (N-[2-((3-(4- bromophenyl)-2-propenyl)-amino)-ethyl]-5-isoquinolinesulfonamide), abolished the enhancement of GJIC by colforsin and IBMX but did not abolish that by isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)