Effect of nitric oxide on calcium-induced calcium release in coronary arterial smooth muscle. Gen Pharmacol 2000 Jul;35(1):37-45
Date
10/27/2001Pubmed ID
11679204DOI
10.1016/s0306-3623(01)00089-1Scopus ID
2-s2.0-0034783876 (requires institutional sign-in at Scopus site) 17 CitationsAbstract
The present study was designed to determine whether nitric oxide (NO)-induced reduction of [Ca(2+)](i) is associated with Ca(2+)-induced Ca(2+) release (CICR) in coronary arterial smooth muscle cells (CASMCs). Caffeine was used as a CICR activator to induce Ca(2+) release in these cells. The effects of NO donor, sodium nitroprusside (SNP), on caffeine-induced Ca(2+) 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 Ca(2+) release with a 330 nM increase in [Ca(2+)](i). Pretreatment of the CASMCs with SNP, CICR inhibitor tetracaine or RYR blocker ryanodine markedly decreased caffeine-induced Ca(2+) release. Addition of caffeine to the Ca(2+)-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 Ca(2+) release and that inhibition of CICR is of importance in mediating the vasodilator response of coronary arteries to NO.
Author List
Li N, Zou AP, Ge ZD, Campbell WB, Li PLAuthor
William B. Campbell PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArteries
Caffeine
Calcium
Cattle
Coronary Vessels
Models, Cardiovascular
Muscle, Smooth, Vascular
Nitric Oxide
Nitroprusside
Oxyhemoglobins
Ryanodine
Tetracaine
Vasoconstriction