Testosterone-induced relaxation involves L-type?and store-operated Ca2+ channels blockade, and PGE2 in guinea pig airway smooth muscle

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• 作者：Mercedes Perusquía ; Edgar Flores-Soto…
• 关键词：Airway smooth muscle ; Testosterone ; Store ; operated Ca2+ channels ; L ; type Ca2+ channels ; PGE2
• 刊名：Pfl篓鹿gers Archiv - European Journal of Physiology
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：467
• 期：4
• 页码：767-777
• 全文大小：1,765 KB
• 参考文献：1. Bazan-Perkins B, Flores-Soto E, Barajas-Lopez C, Monta?o LM (2003) Role of sarcoplasmic reticulum Ca²⁺ content in Ca²⁺ entry of bovine airway smooth muscle cells. Naunyn Schmiedeberg’s Arch Pharmacol 368:277-83
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  13. Flores-Soto E, Reyes-Garcia J, Sommer B, Monta?o LM (2013) Sarcoplasmic reticulum Ca²⁺ refilling is determined by L-type Ca²⁺ and store operated Ca²⁺ channels in guinea pig airway smooth muscle. Eur J Pharmacol 721:21-8
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• 刊物主题：Human Physiology;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-2013

文摘

In vascular smooth muscle, it has been described that testosterone (TES) produces relaxation by blocking L-type Ca2+ channels. Recently, we found that L-type Ca2+ and store-operated Ca2+ (SOC) channels are the main membranal structures that provide extracellular Ca2+ for carbachol (CCh)-induced contraction in airway smooth muscle (ASM). We studied the possible interactions between L-type and SOC channels in TES-induced relaxation in guinea pig ASM. TES (10, 32, 100, and 178?μM) induced a complete relaxation of CCh-precontracted tracheal smooth muscle, and indomethacin partially inhibited this response. In single myocytes, the KCl-induced intracellular Ca2+ increase ([Ca2+]i) was decreased by 32 and completely blocked by 100?nM TES. This androgen (32 and 100?μM) significantly diminished (~25 and 49?%, respectively) the capacitative Ca2+ entry. Myocytes stimulated with CCh produced a transient Ca2+ peak followed by a sustained plateau. D-600 was added during the plateau phase, and a partial diminution (~35?%) was observed. A greater decrease (~78?%) was seen when 2-aminoethyl diphenylborinate (2-APB, SOC antagonist) was used. The combination of both drugs completely abolished the Ca2+ plateau induced by CCh. TES (100?μM) also completely abolished the CCh-induced Ca2+ plateau. Indomethacin significantly diminished this effect of TES. PGE2 and butaprost proportionally decreased the Ca2+ plateau as indomethacin blocked it. Sarcoplasmic reticulum refilling was partially, dependently, and significantly diminished by TES. We concluded that TES-induced relaxation involves blockade of L-type Ca2+ channels at nanomolar and SOC channels at micromolar concentration and PGE2 seems to be also involved in this phenomenon.