Cell-Volume Regulation by Swelling-Activated Chloride Current in Guinea-Pig Ventricular Myocytes

Yamamoto, Shintaro; Ishihara, Keiko; Ehara, Tsuguhisa; Shioya, Takeshi

doi:10.2170/jjphysiol.54.31

Cited by 18 publications

(24 citation statements)

References 26 publications

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“…On the other hand, involvement of I Cl,vol and I Cl,CFTR in regulation of cardiac cell volume has been investigated (25,28). Because I Cl,CFTR is suppressed at acidic pH o (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The investigation conforms also with the Guiding Principles of the Physiological Society of Japan. Single cardiac myocytes from mouse (18 -25 g, C57BL/6J/black inbred, male and female) and guinea pig (250 -350 g, male and female) hearts were isolated with an enzymatic dispersion technique as described previously (25,28,29). The animals were anesthetized with pentobarbital sodium (50 mg/kg ip).…”

Section: Methodsmentioning

confidence: 99%

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Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes

Yamamoto

Ehara²

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Yamamoto, Shintaro, and Tsuguhisa Ehara. Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes. Am J Physiol Heart Circ Physiol 290: H1905-H1914, 2006. First published December 9, 2005 doi:10.1152/ajpheart.00965.2005.-Extracellular acidic pH was found to induce an outwardly rectifying Cl Ϫ current (ICl,acid) in mouse ventricular cells, with a half-maximal activation at pH 5.9. The current showed the permeability sequence for anions to be SCN Ϫ Ͼ Br Ϫ Ͼ I Ϫ Ͼ Cl Ϫ Ͼ F Ϫ Ͼ aspartate, while it exhibited a time-dependent activation at large positive potentials. Similar currents were also observed in mouse atrial cells and in atrial and ventricular cells from guinea pig. Some Cl Ϫ channel blockers (DIDS, niflumic acid, and glibenclamide) inhibited I Cl,acid, whereas tamoxifen had little effect on it. Unlike volume-regulated Cl Ϫ current (I Cl,vol) and CFTR Cl Ϫ current (ICl,CFTR), ICl,acid was independent of the presence of intracellular ATP. Activation of I Cl,acid appeared to be also independent of intracellular Ca 2ϩ and G protein. ICl,acid and I Cl,vol could develop in an additive fashion in acidic hypotonic solutions. Isoprenaline-induced I Cl,CFTR was inhibited by acidification in a pH-dependent manner in guinea pig ventricular cells. Our results support the view that I Cl,acid and ICl,vol stem from two distinct populations of anion channels and that the I Cl,acid channels are present in cardiac cells. I Cl,acid may play a role in the control of action potential duration or cell volume under pathological conditions, such as ischemia-related cardiac acidosis. acidosis; chloride channel; heart CHLORIDE (Cl Ϫ ) channels play a role in a variety of cell functions, such as cell cycle, apoptosis, ion homeostasis, cell volume regulation, and muscle tone (for review see Refs. 11,12,and 20). Several types of Cl Ϫ currents have been recorded in native cardiac cells (for review see Refs. 9 and 11). These include Cl Ϫ currents activated by intracellular PKA (I Cl,PKA ), PKC (I Cl,PKC ), Ca 2ϩ (I Cl,Ca ), extracellular ATP (I Cl,ATP ), or cell swelling (I Cl,vol ) and an inwardly rectifying Cl Ϫ current (I Cl,ir ). The channels responsible for I Cl,PKA , I Cl,PKC , and I Cl,ATP likely share the same molecular basis derived from CFTR gene, and thus these currents can be unified as I Cl,CFTR (11). It has been shown that some of these Cl Ϫ currents depend on extracellular pH (pH o ). Acidic pH o enhances I Cl,Ca in rabbit ventricular cells (10) and I Cl,ir in rat atrial and ventricular cells (13,14) and inhibits I Cl,CFTR in guinea pig ventricular cells (17). The roles of such pH o -dependent attenuation of Cl Ϫ currents in cardiac electrical activity under pathophysiological conditions have been investigated (9 -11, 13, 14).On the other hand, a more directly pH o -dependent regulation has been found in cultured cells. Auzanneau et al. (1) Recently, however, Lambert and Oberwinkler (15) extensively studied the properties of I Cl,acid and I Cl,vol in HEK293 cells. Their import...

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“…On the other hand, involvement of I Cl,vol and I Cl,CFTR in regulation of cardiac cell volume has been investigated (25,28). Because I Cl,CFTR is suppressed at acidic pH o (Fig.…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes

Yamamoto

Ehara²

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…2B). It has been reported that Cl -efflux through VRAC was implicated in RVD in ventricular myocytes (7). Therefore, we examined VRAC currents in ventricular myocytes from shamoperated and TAC-operated mice.…”

Section: Vrac In Cardiac Hypertrophymentioning

confidence: 94%

New Molecular Mechanisms for Cardiovascular Disease: Cardiac Hypertrophy and Cell-Volume Regulation

et al. 2011

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Abstract. Cardiac hypertrophy is an increase in the muscle volume of the ventricle due to the enlargement of cardiac cells. Physiological cardiac hypertrophy is the normal response to healthy exercise, and pathological hypertrophy is the response to increased stress such as hypertension. Intracellular and extracellular aniosmotic conditions also change cell volume. Since persistent cell swelling or cell shrinkage during aniosmotic conditions results in cell death, the ability to regulate cell volume is important for the maintenance of cellular homeostasis. Cell swelling activates a regulatory volume decrease (RVD) response in which solute leakage pathways are stimulated and solute with water exits cells, reducing the cell volume towards the original value. In cardiac cells, one of the essential factors for cell-volume regulation is the volume-regulated anion channel (VRAC). However, the relationship between cardiac hypertrophy and cell-volume regulation is not clear. In this review, we introduce our recent findings showing that the impairment of VRAC current is exhibited in ventricular cells from mice with cardiac hypertrophy induced by transverse aortic constriction. Similar results were shown in caveolin-3-deficient mice, which develop cardiac hypertrophy without pressure overload. These results suggest that VRAC will be a new target for protection from the development of cardiac hypertrophy.

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“…However, the relationship between cardiac hypertrophy and cell-volume regulation is not clear. Yamamoto et al show that the impairment of volumeregulated anion current is exhibited in ventricular cells from mice with cardiac hypertrophy induced by transverse aortic constriction (16). Similar results are observed in caveolin-3-deficient mice, which develop cardiac hypertrophy without pressure overload.…”

Section: +mentioning

confidence: 71%

New Molecular Mechanisms for Cardiovascular Disease: Preface

Iwamoto

Kawasaki

2011

J Pharmacol Sci

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Cell-Volume Regulation by Swelling-Activated Chloride Current in Guinea-Pig Ventricular Myocytes

Cited by 18 publications

References 26 publications

Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes

Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes

New Molecular Mechanisms for Cardiovascular Disease: Cardiac Hypertrophy and Cell-Volume Regulation

New Molecular Mechanisms for Cardiovascular Disease: Preface

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