Effect of nitric oxide on calcium-induced calcium release in coronary arterial smooth muscle

The present study was designed to determine whether nitric oxide (NO)-induc ed reduction of [Ca2+](i) is associated with Ca2+-induced Ca2+ release (CIC R) in coronary arterial smooth muscle cells (CASMCs). Caffeine was used as a CICR activator to induce Ca2+ release in these cells. The effects of NO d onor, sodium nitroprusside (SNP), on caffeine-induced Ca2+ release were exa mined in freshly dissociated bovine CASMCs using single cell fluorescence m icroscopic spectrometry. The effects of NO donor on caffeine-induced corona ry vasoconstriction were examined by isometric tension recordings. Caffeine , a CICR or ryanodine receptor (RYR) activator, produced a rapid Ca2+ relea se with a 330 nM increase in [Ca2+](i). Pretreatment of the CASMCs with SNP , CICR inhibitor tetracaine or RYR blocker ryanodine markedly decreased caf feine-induced Ca2+ release. Addition of caffeine to the Ca2+-free bath solu tion produced a transient coronary vasoconstriction. SNP, tetracame and rya nodine, but not guanylyl cyclase inhibitor, ODQ, significantly attenuated c affeine-induced vasoconstriction. These results suggest that CICR is functi oning in CASMCs and participates in the vasoconstriction in response to caf feine-induced Ca2+ release and that inhibition of CICR is of importance in mediating the vasodilator response of coronary arteries to NO. (C) 2001 Els evier Science Inc. All rights reserved.