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

Abstract

The present study was designed to determine whether nitric oxide (NO)-induced reduction of [Ca²⁺]_i is associated with Ca²⁺-induced Ca²⁺ release (CICR) 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 donor, sodium nitroprusside (SNP), on caffeine-induced Ca²⁺ release were examined in freshly dissociated bovine CASMCs using single cell fluorescence microscopic spectrometry. The effects of NO donor on caffeine-induced coronary vasoconstriction were examined by isometric tension recordings. Caffeine, a CICR or ryanodine receptor (RYR) activator, produced a rapid Ca²⁺ release with a 330 nM increase in [Ca²⁺]_i. Pretreatment of the CASMCs with SNP, CICR inhibitor tetracaine or RYR blocker ryanodine markedly decreased caffeine-induced Ca²⁺ release. Addition of caffeine to the Ca²⁺-free bath solution produced a transient coronary vasoconstriction. SNP, tetracaine and ryanodine, but not guanylyl cyclase inhibitor, ODQ, significantly attenuated caffeine-induced vasoconstriction. These results suggest that CICR is functioning in CASMCs and participates in the vasoconstriction in response to caffeine-induced Ca²⁺ release and that inhibition of CICR is of importance in mediating the vasodilator response of coronary arteries to NO.