HCO3 dependent impact of Na+,K+, 2Cl cotransport in vascular smooth muscle excitation-contraction coupling
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31 octobre 2022
- handle: 10670/1.h8axlf
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Muscle, Vascular Blood-vessels--MusclesCiter ce document
Svetlana V. Koltsova et al., « HCO3 dependent impact of Na+,K+, 2Cl cotransport in vascular smooth muscle excitation-contraction coupling », Papyrus : le dépôt institutionnel de l'Université de Montréal, ID : 10670/1.h8axlf
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In smooth muscles, inhibition of Na(+),K(+),2Cl(-) cotransport (NKCC) by bumetanide decreased intracellular Cl(-) content ([Cl(-)](i)) and suppressed the contractions triggered by diverse stimuli. This study examines whether or not bicarbonate, a regulator of several Cl(-) transporters, affects the impact of NKCC in excitation-contraction coupling. Addition of 25 mM NaHCO(3) attenuated the inhibitory action of bumetanide on mesenteric artery contractions evoked by 30 mM KCl and phenylephrine (PE) by 5 and 3-fold, respectively. In cultured vascular smooth muscle cells, NaHCO(3) almost completely abolished inhibitory actions of bumetanide on transient depolarization and [Ca(2+)](i) elevation triggered by PE. In bicarbonate-free medium, bumetanide decreased [Cl(-)](i) by approximately 15%; this effect was almost totally abrogated by NaHCO(3). The addition of NaHCO(3) resulted in 2-fold inhibition of NKCC activity and 3-fold attenuation of [Cl(-)](i). These data strongly suggest that extracellular HCO(3)(-) diminishes the NKCC-sensitive component of excitation-contraction coupling via suppression of this carrier.