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Endothelin-1 increases intracellular Ca²⁺ in rabbit pulmonary artery smooth muscle cells through phospholipase C

¹Department of Physiology and National Research Laboratory for Cellular Signalling, Seoul National University College of Medicine, Seoul; and ²Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Biohealth Products Research Center, Cardiovascular and Metabolic Disease Center, Inje University, Busan, Korea

Submitted 9 February 2005 ; accepted in final form 26 May 2005

In freshly isolated rabbit pulmonary artery smooth muscle cells, endothelin (ET)-1 induced a transient increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) followed by a return to the initial [Ca²⁺]_i. This response was not abolished by the voltage-dependent Ca²⁺ channel blocker nicardipine or removal of Ca²⁺ from the bath solution but was inhibited by ryanodine and thapsigargin. This finding suggested that the increase in [Ca²⁺]_i induced by ET-1 was attributable to release of Ca²⁺ from ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca²⁺ stores. The transient increase in [Ca²⁺]_i induced by ET-1 was also inhibited by pretreatment with antagonists of ET type A and B (ET_A and ET_B) receptors (BQ-123 and BQ-788, respectively). Furthermore, the ET_B receptor agonist IRL-1620 induced an increase in [Ca²⁺]_i that was followed by a sustained increase in [Ca²⁺]_i; the sustained increase in [Ca²⁺]_i was blocked by nicardipine. Using the nystatin-perforated patch-clamp technique, we found that IRL-1620 caused an increase in Ca²⁺ current that was inhibited by addition of ET-1. ET-1 did not inhibit Ca²⁺ current when cells were pretreated with BQ-123. These results suggested that when both receptor types are activated, the opposing responses lead to abolition of the sustained [Ca²⁺]_i increases induced by ET_B receptor activation. Western blot analysis confirmed expression of ET_A and ET_B receptors. Finally, U-73122 inhibited the ET-1-induced [Ca²⁺]_i increase, indicating that phospholipase C was involved in modulation of the ET-1-induced [Ca²⁺]_i increase in rabbit pulmonary artery smooth muscle cells.

endothelin receptors; voltage-dependent Ca²⁺ channel

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