AIM: To study the effect of superoxide anion on the Ca2+ homeostasis in smooth muscle cells isolated from the rabbit pulmonary artery. METHODS: Intracellular Ca2+ concentration ([Ca2+](i)) was investigated using cell suspension of freshly isolated smooth muscle cells from rabbit pulmonary artery (PASMC). Fura-2 fluorescent ratio obtained at 340 nm and 380 nm wave lengths was measured as an indicator of [Ca2+](i). RESULTS: ATP 30 μmol·L-1 induced a transient increase in the ratio (Ca2+ transient). Thapsigargin, an inhibitor of sarcoplasmic Ca2+ ATPase, induced a phasic increase in the ratio due to Ca2+ leak from intracellular store sites, but not the sustained increase, thereby suggesting the absence of Ca2+ release- activated Ca2+ entry (CRAC) mechanism in PASMC. When PASMC were exposed to superoxide anion by the pretreatment with xanthine and xanthine oxidase (X/XO) for 30 min, sustained component of ATP-induced Ca2+ transient was elevated. The ratios at 5 and 10 min after ATP application (Δratio5 (min) and Δratio10(min)) were increased from 0.091 ± 0.022 to 0.149 ± 0.048 (P < 0.05) and from 0.021 ± 0.020 to 0.117 ± 0.047 (P < 0.01), respectively. But, thapsigargin-induced [Ca2+](i) transient was not affected by X/XO. CONCLUSION: Superoxide anion makes ATP induced Ca2+ transient sluggish, and does not affect Ca2+ leak pathway in PASMC.
|Number of pages||5|
|Journal||Acta Pharmacologica Sinica|
|Publication status||Published - Jan 27 1999|
All Science Journal Classification (ASJC) codes
- Pharmacology (medical)