Store-operated Ca2+ influx in airway smooth muscle - Interactions between volatile anesthetic and cyclic nucleotide effects

Prakash Y. S., Iyanoye A., Ay B., Sieck G. C., Pabelick C. M.

ANESTHESIOLOGY, vol.105, no.5, pp.976-983, 2006 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 105 Issue: 5
  • Publication Date: 2006
  • Doi Number: 10.1097/00000542-200611000-00019
  • Journal Name: ANESTHESIOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.976-983
  • Marmara University Affiliated: No

Abstract

Background Volatile anesthetics produce bronchodilation in part by depleting sarcoplasmic reticulum Ca2+ stores in airway smooth muscle (ASM). Other bronchodilatory drugs are known to act via cyclic nucleotides (cyclic adenosine 3',5'-cyclic monophosphate, cyclic guanosine 3',5'-cyclic monophosphate). Intracellular Ca2+ regulation in ASM involves plasma membrane Ca2+ influx, including that triggered by sarcoplasmic reticulum Ca2+ depletion (store-operated Ca2+ entry [SOLED. The authors hypothesized that anesthetics and bronchodilatory agents interact in inhibiting SOLE, thus enhancing ASM relaxation.