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

Ningjun Li, Ai Ping Zou, Zhi-Dong Ge, William B. Campbell, Pin Lan Li*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)37-45
Number of pages9
JournalGeneral Pharmacology: The Vascular System
Issue number1
StatePublished - Jul 2000


  • Ca-induced Ca release
  • Calcium mobilization
  • Coronary artery
  • Endothelium-derived relaxing factor
  • Heart
  • Vascular tone

ASJC Scopus subject areas

  • Pharmacology

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