Erratum to The three mechanisms of intracellular chloride accumulation in vascular smooth muscle of human umbilical and placental arteries

Davis, Junior; Chien, Patrick; Chipperfield, A. R.; Gordon, A. J.; Harper, A. A.

doi:10.1007/s004240000452

Cited by 14 publications

(8 citation statements)

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“…Pump III is a mechanism for accumulating intracellular Cl -content that still has activity, even though inhibiting the activation of Cl -/HCO 3 -exchanger and (Na + +K + +Cl -) cotransporter. It has been shown that DIDS (100 µM), bumetanide (10 µM), and acetazolamide (1 mM) inhibit Cl -/HCO 3 -exchange, (Na + +K + +Cl -) cotransport, and pump III, respectively, in human umbilical and placental arteries [6]. In the present study, the I-154 K + solution containing DIDS (100 µM), but not bumetanide (10 µM) or acetazolamide (1 mM), induced a well-maintained contraction and significantly decreased the ratio of cellular water content.…”

Section: Discussionmentioning

confidence: 99%

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Kaneda

SAKAGUCHI

Shimizu

et al. 2006

The Journal of Veterinary Medical Science

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ABSTRACT. A high-K + , Na + -deficient (I-154 K + ) solution induced contraction followed by gradual relaxation of the smooth muscles of the bovine trachea, while hyperosmotic addition of 65 mM KCl induced a large sustained contraction. Exposure of the muscle to the I-154 K + solution induced an increase in the ratio of cellular water content and a sustained increase in oxidized flavoprotein fluorescence or reduced pyridine nucleotide fluorescence. The I-154 K + solution also induced a sustained increase in [Ca 2+ ]i level. Decreases in developed tension and increases in cellular water content were both prevented by the addition of sucrose or NaCl but not pyruvate. Substitution of KI for KCl in the I-154 K + solution produced a greater inhibition of contraction, while substitution with K-propionate produced no inhibition of contraction. Moreover, decreases in developed tension and increases in cellular water content were both prevented by addition of 100 µM 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS), but not 10 µM bumetanide or 1 mM acetazolamide. In conclusion, I-154 K + solution induced-relaxation in the bovine trachea may be due to swelling of smooth muscle cells and the mechanism of swelling is probably involved in DIDS-sensitive anion movement.

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Section: Discussionmentioning

confidence: 99%

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Kaneda

SAKAGUCHI

Shimizu

et al. 2006

The Journal of Veterinary Medical Science

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“…Full extracellular Cl Ϫ replacement rapidly shifts E Cl from approximately -35 to Ϫ40 mV to a positive value, which provides a strong driving force for Cl Ϫ exit from the cell, and, if Cl Ϫ conductance is open, rapid and transient depolarization ensues. When blood vessels are challenged by Cl Ϫ -free conditions, intracellular Cl Ϫ concentration has been measured to approach nominal levels, i.e., Ϸ4 mM (likely reflecting the level of electrode interference from other intracellular anions) within 5 min and remain there (10,11). Thus, with prolonged absence of extracellular Cl Ϫ , intracellular Cl Ϫ concentration levels will be negligible as the anion membrane transporters are unable to replenish this anion in the cell, and despite a very positive E Cl , cellular Cl Ϫ conductances become physiologically antagonized.…”

Section: Functional Datamentioning

confidence: 99%

Spontaneous and α-adrenoceptor-induced contractility in human collecting lymphatic vessels require chloride

Mohanakumar

Majgaard

Telinius

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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Human lymphatic vessels are myogenically active and respond to sympathetic stimulation. The role of various cations in this behavior has recently been investigated, but whether the anion Cl is essential is unclear. With ethical approval and informed consent, human thoracic duct and mesenteric lymphatic vessels were obtained from surgical patients. Spontaneous or norepinephrine-induced isometric force production from isolated vessels was measured by wire myography; the transmembrane Cl gradient and Cl channels were investigated by substitution of extracellular Cl with the impermeant anion aspartate and inhibition of Cl transport and channels with the clinical diuretics furosemide and bendroflumethiazide as well as DIDS and 5-nitro-2-(3-phenylpropylamino)benzoic acid. The molecular expression of Ca-activated Cl channels was investigated by RT-PCR, and proteins were localized using immunoreactivity. Spontaneous and norepinephrine-induced contractility in human lymphatic vessels was highly abrogated after Cl substitution with aspartate. About 100-300 µM DIDS or 5-nitro-2-(3-phenylpropylamino)benzoic acid inhibited spontaneous contractile behavior. Norepinephrine-stimulated tone was furthermore markedly abrogated by 200 µM DIDS. Furosemide lowered only spontaneous constrictions, whereas bendroflumethiazide had nonspecific inhibitory effects. Consistent expression of transmembrane member 16A [TMEM16A (anoctamin-1)] was found in both the thoracic duct and mesenteric lymphatic vessels, and immunoreactivity with different antibodies localized TMEM16A to lymphatic smooth muscle cells and interstitial cells. The significant change in contractile function observed with inhibitors and anion substitution suggests that Cl movement over the plasma membrane of lymphatic myocytes is integral for spontaneous and α-adrenoceptor-evoked contractility in human collecting lymphatic vessels. Consistent detection and localization of TMEM16A to myocytes suggests that this channel could play a major functional role. NEW & NOTEWORTHY In this study, we report the first observations of Cl being a critical ionic component of spontaneous and agonist-evoked contractility in human lymphatics. The most consistently expressed Ca-activated Cl channel gene in the human thoracic duct and mesenteric lymphatic vessels appears to be transmembrane member 16A, suggesting that this channel plays a major role.

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“…The first discovered of these is the anion exchanger, which mediates an electroneutral exchange of Cl Ϫ for HCO 3 Ϫ . In VSMC, this transporter is involved in maintaining a high intracellular chloride concentration, 9 and during intracellular alkalinization it is activated to participate in the regulation of pH i . 10 The first anion exchanger (AE1) was cloned 20 years ago from erythrocytes, 11 and in VSMC the transporter is also well defined at the molecular level: AE2 is predominant together with smaller amounts of AE3.…”

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confidence: 99%

NBCn1 (slc4a7) Mediates the Na ⁺ -Dependent Bicarbonate Transport Important for Regulation of Intracellular pH in Mouse Vascular Smooth Muscle Cells

Boedtkjer¹,

Prætorius²,

Aalkjær³

2006

Circulation Research

151

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The contribution of sodium-dependent bicarbonate transport to intracellular pH (pH(i)) regulation in vascular smooth muscle cells is controversial, partly because the molecular identity of the transporter(s) responsible has not been identified. Here, using the pH-sensitive fluorophore 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF), we show that smooth muscle cells of intact mouse mesenteric, coronary, and cerebral small arteries all display a sodium- and bicarbonate-dependent pH(i) recovery after an NH4+-prepulse. The sodium-dependent bicarbonate flux was largely 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) sensitive (56% to 91%) and of a magnitude similar to the amiloride-sensitive flux. Additionally, steady-state pH(i) was lower (0.2 to 0.4 pH units magnitude) in all 3 vascular beds when CO2/bicarbonate was omitted. RT-PCR analyses showed that NBCn1 (slc4a7) is the only Na+-dependent bicarbonate transporter of the slc4 family detectable at the mRNA level in all 3 vascular beds investigated. Whole-mount immunolabeling and immunogold electron microscopy confirmed the presence of NBCn1 protein in the sarcolemma of mouse mesenteric small arterial smooth muscle cells. Intact mouse mesenteric small arteries were electropermeated to facilitate transfection with small interfering RNA targeting NBCn1, which resulted in an approximate 43% decrease in the ratio of NBCn1 to glyceraldehyde-3-phosphate dehydrogenase mRNA. After knock-down, we found a decreased steady-state pH(i) (0.21+/-0.08 pH units) as well as a 68+/-10% decrease in the net Na+-dependent, amiloride-insensitive base influx after acid load. Finally, omission of CO2/bicarbonate resulted in a decreased contractile response to norepinephrine after sustained exposure to the agonist, underlining the importance of CO2/bicarbonate for vascular contractility. We conclude that NBCn1 mediates the Na+-dependent bicarbonate transport important for pH(i) regulation in smooth muscle cells of mouse mesenteric, coronary, and cerebral small arteries.

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Erratum to The three mechanisms of intracellular chloride accumulation in vascular smooth muscle of human umbilical and placental arteries

Cited by 14 publications

References 0 publications

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Spontaneous and α-adrenoceptor-induced contractility in human collecting lymphatic vessels require chloride

NBCn1 (slc4a7) Mediates the Na ⁺ -Dependent Bicarbonate Transport Important for Regulation of Intracellular pH in Mouse Vascular Smooth Muscle Cells

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Erratum to The three mechanisms of intracellular chloride accumulation in vascular smooth muscle of human umbilical and placental arteries

Cited by 14 publications

References 0 publications

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Effects of High-K+, Na+-Deficient Solution on Contractility of the Smooth Muscles of the Bovine Trachea

Spontaneous and α-adrenoceptor-induced contractility in human collecting lymphatic vessels require chloride

NBCn1 (slc4a7) Mediates the Na + -Dependent Bicarbonate Transport Important for Regulation of Intracellular pH in Mouse Vascular Smooth Muscle Cells

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NBCn1 (slc4a7) Mediates the Na ⁺ -Dependent Bicarbonate Transport Important for Regulation of Intracellular pH in Mouse Vascular Smooth Muscle Cells