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Mesaconitine-induced Relaxation in Rat Aorta: Role of Na+/Ca2+ Exchangers in Endothelial Cells

Mesaconitine-induced Relaxation in Rat Aorta: Role of Na+/Ca2+ Exchangers in Endothelial Cells

Junko Ogura, Mana Mitamura, Akiyoshi Someya, Ken Shimamura, Hiromitsu Takayama, Norio Aimi, Syunji Horie, Toshihiko Murayama

Eur J Pharmacol. 2004 Jan 12;483(2-3):139-46.

PMID: 14729101

Abstract:

Previously, we reported that mesaconitine, an aconite alkaloid, increased intracellular Ca(2+) concentration ([Ca(2+)](i)) level in endothelium and caused relaxation in rat aorta via nitric oxide production. In the present study, we investigated the mechanisms of increase in the [Ca(2+)](i) level induced by mesaconitine in rat aorta and in human umbilical vein endothelial cells (HUVECs). Treatment with the low Na(+) buffer delayed the 30 microM mesaconitine-, but not 10 microM acetylcholine-, induced relaxation in rat aorta. Treatments with an inhibitor of Na(+)/Ca(2+) exchangers (20 microM 3',4'-dichlorobenzamil) and a reversed mode (Ca(2+) influx) inhibitor of the exchangers (30 microM 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate, KBR7943) showed similar effects. In HUVECs, 30 microM mesaconitine increased the [Ca(2+)](i) level in the presence of extracellular CaCl(2) and NaCl, and the response was inhibited by KBR7943. Mesaconitine increased intracellular Na(+) concentration level in HUVECs. The [Ca(2+)](i) response by mesaconitine was inhibited by 100 microM D-tubocurarine (an inhibitor of nicotinic acetylcholine receptors), but was not inhibited in the glucose-free buffer and by inhibitors of Na(+)/H(+) exchangers. These findings suggest that mesaconitine stimulated Ca(2+) influx via the Na(+)/Ca(2+) exchangers in endothelial cells and caused relaxation in the aorta. The possibility of D-tubocurarine-sensitive Na(+) channels as target(s) of mesaconitine is discussed.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP2752649	Mesaconitine		2752-64-9	Price

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