Release of Ca<sup>2+</sup> from the sarcoplasmic reticulum increases mitochondrial [Ca<sup>2+</sup>] in rat pulmonary artery smooth muscle cells

Drummond, Robert M.; Tuft, Richard A.

doi:10.1111/j.1469-7793.1999.139aa.x

Cited by 104 publications

(84 citation statements)

References 45 publications

(92 reference statements)

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“…For PASMC isolation, the heart and lungs were removed en bloc and placed in a dissecting solution of the following composition (in mM): NaCl 119, KCl 4.7, KH 2 PO 4 1.18, MgSO 4 1.17, glucose 5.5, NaHC0 3 25, HEPES 10, pH adjusted to 7 Á 4 with NaOH. Thereafter, intrapulmonary arteries (400 -800 mm outside diameter) were dissected out and PASMCs isolated using the method previously described by Drummond & Tuft (1999). Briefly, arterial ring segments (B1 mm in length) were placed in a dissociation solution of the following composition (mM): NaCl 128, KCl 5.4, KH 2 PO 4 0.95, Na 2 HPO 4 0.35, MgSO 4 1.17, glucose 10, sucrose 2.9, NaHCO 3 4.16, HEPES 10, pH adjusted to 7.3 with NaOH.…”

Section: Cell Isolationmentioning

confidence: 99%

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

Cruickshank

Baxter

Drummond

2003

British J Pharmacology

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1 The effect of the Cl À channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4 0 -diisothiocyanatostilbene-2,2 0 -disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca 2 þ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca 2 þ concentration ([Ca 2 þ ] i ) was monitored with either fura-2 or fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca 2 þ from the sarcoplasmic reticulum (SR). 2 NFA and NPPB significantly increased basal [Ca 2 þ ] i and attenuated the caffeine-induced increase in [Ca 2 þ ] i . These Cl À channel blockers also increased the half-time (t 1/2 ) to peak for the caffeineinduced [Ca 2 þ ] i transient, and slowed the removal of Ca 2 þ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, fluo-4 was used to monitor intracellular Ca 2 þ in studies involving these Cl À channel blockers. Both DIDS and A-9-C increased basal fluo-4 fluorescence, indicating an increase in intracellular Ca 2 þ , and while DIDS had no significant effect on the t 1/2 to peak for the caffeine-induced Ca 2 þ transient, it was significantly increased by A-9-C. 3 In the absence of extracellular Ca 2 þ , NFA significantly increased basal [Ca 2 þ ] i , suggesting that the release of Ca 2 þ from an intracellular store was responsible for the observed effect. 4 Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca 2 þ ] i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca 2 þ ] i induced by NFA. 5 These data show that Cl À channel blockers have marked effects on Ca 2 þ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca 2 þ ] i indicates that it is likely due to Ca 2 þ release from an intracellular store, most probably the SR.

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Section: Cell Isolationmentioning

confidence: 99%

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

Cruickshank

Baxter

Drummond

2003

British J Pharmacology

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“…Besides being a possible trigger organelle, mitochondria can be a modulator of HPV. In particular, calcium homeostasis of the cell is regulated by mitochondria, by calcium buffering [127][128][129] and regulating capacitative calcium entry [130].…”

Section: Mitochondria In the Cellmentioning

confidence: 99%

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

Sommer¹,

Dietrich²,

Schermuly³

et al. 2008

Eur Respir J

186

148

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Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure.Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised vasoconstriction of the pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltagedependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of hypoxic pulmonary vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate.In this context the present article focuses on the basic mechanisms of hypoxic pulmonary vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of hypoxic pulmonary vasoconstriction.

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“…In smooth muscle cells, as well as other cell types, mitochondrial Ca 2ϩ sequestration and release influences spatial and temporal patterns of Ca 2ϩ transients in the cytoplasm (8,9,11,24,25). There is evidence that membrane currents and cytosolic Ca 2ϩ oscillations correspond to mitochondrial Ca 2ϩ oscillations in isolated GI and vascular smooth muscle cells (8,9,25).…”

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confidence: 99%

Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle

Balemba

Bartoo²,

Nelson³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Release of Ca²⁺ from the sarcoplasmic reticulum increases mitochondrial [Ca²⁺] in rat pulmonary artery smooth muscle cells

Abstract: 1. The Ca¥-sensitive fluorescent indicator rhod_2 was used to measure mitochondrial [Ca¥] (

Cited by 104 publications

References 45 publications

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle

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Release of Ca2+ from the sarcoplasmic reticulum increases mitochondrial [Ca2+] in rat pulmonary artery smooth muscle cells

Abstract: 1. The Ca¥-sensitive fluorescent indicator rhod_2 was used to measure mitochondrial [Ca¥] (

Cited by 104 publications

References 45 publications

The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle

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Release of Ca²⁺ from the sarcoplasmic reticulum increases mitochondrial [Ca²⁺] in rat pulmonary artery smooth muscle cells

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells