HCO(3)-Dependent Impact of Na(+),K(+),2Cl(-) Cotransport in Vascular Smooth Muscle Excitation-Contraction Coupling. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology [Cell Physiol Biochem] Journal article | | Title | HCO(3)-Dependent Impact of Na(+),K(+),2Cl(-) Cotransport in Vascular Smooth Muscle Excitation-Contraction Coupling. | | Author(s) | Koltsova SV, Luneva OG, Lavoie JL, Tremblay J, Maksimov GV, Hamet P, Orlov SN | | Institution | Research Centre, Centre hospitalier de l'Université de Montréal, (CHUM) - Technopôle Angus, Montreal (Canada). | | Source | Cell Physiol Biochem 2009; 23(4-6):407-414. | | Abstract | 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. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19471108 |
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