Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Laporte, Régent; Hui, Adrian; Laher, Ismail

doi:10.1124/pr.56.4.1

Cited by 89 publications

(108 citation statements)

References 707 publications

(753 reference statements)

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“…In addition this is in the range of concentration of 2-APB used in our ex vivo experiments with isolated pulmonary arteries. Other potential actions of 2-APB different than SOC inhibition must be considered, such as inhibition of inositol-(1,4,5)-triphosphate-dependent calcium release (29), of TRPM7 channels [a type of Mg-inhibitable cation channel (2)], of gap junction intercellular communications (23), and of mitochondrial calcium efflux, as well as potentiation and inhibition of store-operated currents, depending on the concentration of the drug (39), are described in other experimental models. However, we had similar results with SKF-96365, another SOC blocker, in the relaxation of the isolated small pulmonary arteries, suggesting that the main 2-APB effect is to block these channels.…”

Section: Discussionmentioning

confidence: 99%

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Parrau

Ebensperger

Herrera

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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AJ, Reyes RV. Store-operated channels in the pulmonary circulation of high-and low-altitude neonatal lambs. Am J Physiol Lung Cell Mol Physiol 304: L540 -L548, 2013. First published February 15, 2013 doi:10.1152/ajplung.00024.2012.-We determined whether store-operated channels (SOC) are involved in neonatal pulmonary artery function under conditions of acute and chronic hypoxia, using newborn sheep gestated and born either at high altitude (HA, 3,600 m) or low altitude (LA, 520 m). Cardiopulmonary variables were recorded in vivo, with and without SOC blockade by 2-aminoethyldiphenylborinate (2-APB), during basal or acute hypoxic conditions. 2-APB did not have effects on basal mean pulmonary arterial pressure (mPAP), cardiac output, systemic arterial blood pressure, or systemic vascular resistance in both groups of neonates. During acute hypoxia 2-APB reduced mPAP and pulmonary vascular resistance in LA and HA, but this reduction was greater in HA. In addition, isolated pulmonary arteries mounted in a wire myograph were assessed for vascular reactivity. HA arteries showed a greater relaxation and sensitivity to SOC blockers than LA arteries. The pulmonary expression of two SOC-forming subunits, TRPC4 and STIM1, was upregulated in HA. Taken together, our results show that SOC contribute to hypoxic pulmonary vasoconstriction in newborn sheep and that SOC are upregulated by chronic hypoxia. Therefore, SOC may contribute to the development of neonatal pulmonary hypertension. We propose SOC channels could be potential targets to treat neonatal pulmonary hypertension.hypoxia; pulmonary vasoconstriction; pulmonary hypertension; 2-aminoethydiphenylborinate; pulmonary vascular reactivity PULMONARY ARTERIES HAVE AN intrinsic vasoconstrictor response to low oxygen levels when exposed to acute hypoxia. This is a reversible, rapid and physiological response, known as hypoxic pulmonary vasoconstriction (HPV), that redirects blood flow from poorly oxygenated to better oxygenated alveoli. Thus, when total lung is exposed to hypoxia, HPV results in an increase in pulmonary artery pressure (PAP) that reverses when normoxia is reestablished (31). However, exposure to chronic hypoxia produces an imbalance between vasodilator and vasoconstrictor mechanisms, and there is pulmonary vascular remodeling that includes proliferation of pulmonary artery myocytes among other cellular processes (46). The result is a pathological and persistent increase in pulmonary artery contractile tone and pulmonary arterial hypertension, which in many cases leads to right ventricular hypertrophy, right heart failure, and eventually death (13).In pulmonary artery smooth muscle cells, an increase in intracellular calcium concentration ([Ca 2ϩ ] i ) is essential for HPV, proliferation, and remodeling (13,19,20,42). This increase in [Ca 2ϩ ] i greatly depends on an influx of extracellular calcium (13, 59), which may enter the smooth muscle cell through store-operated channels (SOC) among other pathways (5,8,22,40). These are channels physiologically ...

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Section: Discussionmentioning

confidence: 99%

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Parrau

Ebensperger

Herrera

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Either of these events, which cause an initial rise in [Ca 2+ ]i, may be further augmented by ryanodine receptor (RyR)-mediated Ca 2+ release activated via a Ca 2+ -induced Ca 2+ release (CICR) mechanism (Fabiato and Fabiato, 1975). However, the recruitment of RyR-mediated Ca 2+ release by voltage-gated Ca 2+ entry and/or IP3R-mediated Ca 2+ release in smooth muscles is still an area of extensive debate and controversy (reviewed in Laporte et al, 2004;Wray and Burdyga, 2010). Indeed, the relative contribution of RyRs and IP3Rs to intracellular [Ca 2+ ]i mobilization varies in different types of SMCs, and often depends on the strengths and mechanism of SMC stimulation.…”

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confidence: 99%

Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries

Povstyan

Harhun

Gordienko

2011

British J Pharmacology

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BACKGROUND AND PURPOSEP2X receptors mediate sympathetic control and autoregulation of the renal circulation triggering contraction of renal vascular smooth muscle cells (RVSMCs) via an elevation of intracellular Ca 2+ concentration ([Ca 2+ ]i). Although it is well-appreciated that the myocyte Ca 2+ signalling system is composed of microdomains, little is known about the structure of the [Ca 2+ ]i responses induced by P2X receptor stimulation in vascular myocytes. EXPERIMENTAL APPROACHESUsing confocal microscopy, perforated-patch electrical recordings, immuno-/organelle-specific staining, flash photolysis and RT-PCR analysis we explored, at the subcellular level, the Ca 2+ signalling system engaged in RVSMCs on stimulation of P2X receptors with the selective agonist ab-methylene ATP (ab-meATP). KEY RESULTSRT-PCR analysis of single RVSMCs showed the presence of genes encoding inositol 1,4,5-trisphosphate receptor type 1(IP3R1) and ryanodine receptor type 2 (RyR2). The amplitude of the [Ca 2+ ]i transients depended on ab-meATP concentration. Depolarization induced by 10 mmol·L -1 ab-meATP triggered an abrupt Ca 2+ release from sub-plasmalemmal ('junctional') sarcoplasmic reticulum enriched with IP3Rs but poor in RyRs. Depletion of calcium stores, block of voltage-gated Ca 2+ channels (VGCCs) or IP3Rs suppressed the sub-plasmalemmal [Ca 2+ ]i upstroke significantly more than block of RyRs. The effect of calcium store depletion or IP3R inhibition on the sub-plasmalemmal [Ca 2+ ]i upstroke was attenuated following block of VGCCs. CONCLUSIONS AND IMPLICATIONSDepolarization of RVSMCs following P2X receptor activation induces IP3R-mediated Ca 2+ release from sub-plasmalemmal ('junctional') sarcoplasmic reticulum, which is activated mainly by Ca 2+ influx through VGCCs. This mechanism provides convergence of signalling pathways engaged in electromechanical and pharmacomechanical coupling in renal vascular myocytes. Abbreviations2-APB, 2-aminoethoxydiphenyl borate; ab-meATP, ab-methylene ATP; CICR, Ca 2+ -induced Ca 2+ release; CPA, cyclopiazonic acid; IP3, inositol 1,4,5-trisphosphate; IP3R, inositol 1,4,5-trisphosphate receptor; jSR, sub-plasmalemmal ('junctional') sarcoplasmic reticulum; MRS2578, N,N' NF279, 8,] bis(1,3,5-naphthalene-trisulphonic acid); PLC, phospholipase C; RBF, renal blood flow; RSNA, renal sympathetic nerve activity; RT-PCR, reverse transcription polymerase chain reaction; RVSMC, renal vascular smooth muscle cells; RyR, ryanodine receptor; SERCA, sarco-/endoplasmic reticulum Ca 2+ -ATPase; SPCU, sub-plasmalemmal [Ca 2+ ]i upstroke; SR, sarcoplasmic reticulum; U-73122, 1-[6-([(17b)-3-methoxyestra-1,3,5(10) IntroductionRenal blood flow (RBF) accounts for 20-25% of cardiac output at rest (Malpas and Leonard, 2000;Cupples and Braam, 2007). The mechanisms controlling contraction/relaxation of renal vascular smooth muscle cells (RVSMCs), which regulate the diameter of renal resistance arteries and hence RBF and glomerular filtration rate, play a fundamental role in the control of systemic blood pr...

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“…Studies (22,23) in other muscle types have indicated that SERCA activity influences contractile behavior by modulating the rate of Ca 2ϩ clearance from the cytosol and the rate of subsequent SR Ca 2ϩ release. When cytosolic Ca 2ϩ removal is inhibited by CPA, more Ca 2ϩ is available for contraction (31). In addition, when SR Ca 2ϩ refilling is inhibited by CPA, less Ca 2ϩ is available for release (20).…”

Section: Discussionmentioning

confidence: 99%

CaM kinase II activation and phospholamban phosphorylation by SNP in murine gastric antrum smooth muscles

Kim

Perrino²

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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and Thr 17 phosphorylation were ODQ sensitive. However, only PLBThr 17 phosphorylation was inhibited by CPA or KN-93. These results suggest that CaM kinase II activation and PLB phosphorylation participate in the relaxant effect of SNP on murine gastric antrum smooth muscles through a nitric oxide/guanylyl cyclase/cGMP pathway. Ca 2ϩ /calmodulin-dependent protein kinase II; phospholamban; nitric oxide THE GASTRIC ANTRUM undergoes spontaneous peristaltic contractions to accomplish the grinding, mixing, and gastric emptying functions of this part of the stomach. Slow wave propagation from the greater curvature of the orad corpus to the pylorus produces gastric peristalsis. Phasic contractions initiated by slow waves are the basis for gastric peristalsis (25). The normal pattern of slow wave propagation results from a gradient in intrinsic frequencies along the longitudinal axis of the stomach. The orad corpus is the dominant pacemaker in the human stomach and in animal models such as the dog and mouse (12,25,38) because it generates slow waves at the fastest rate. Conditions that affect the intrinsic pacemaker frequency in the antrum or produce arrhythmic activity in this region can result in a breakdown in functional coupling between the corpus and antrum and interfere with normal gastric emptying (6, 26).Insufficient gastric emptying produces pathophysiological problems such as functional dyspepsia, postsurgical gastroparesis, and diabetic gastroparesis (29, 51). Slow wave generation by myenteric interstitial cells of Cajal results in the activation of voltage-dependent Ca 2ϩ channels and the generation of phasic contractions of antrum smooth muscle cells (9,11,39,40). Thus, in addition to studies of the electrical coupling of myenteric interstitial cells of Cajal to smooth muscle cells, studies of the Ca 2ϩ -handling mechanisms of antrum smooth muscles will provide insights into gastric smooth muscle physiology and pathophysiology.The relaxant effects of nitric oxide (NO) and NO donors on smooth muscles are well established, but many details of the mechanism of NO-induced relaxation are still under investigation (54). One possible mechanism by which NO relaxes smooth muscle is by hyperpolarization of the smooth muscle cell plasma membrane. Porter et al. (43) reported that the NO donor sodium nitroprusside (SNP) increases Ca 2ϩ spark frequency and activates spontaneous transient outward currents (STOCs) via a NO/soluble guanylyl cyclase (sGC)/cGMP pathway in cerebral and coronary artery myocytes. Furthermore, SNP-induced relaxation of the rat gastric fundus is ryanodine sensitive and involves small-conductance Ca 2ϩ -activated K ϩ (K Ca ) channels (15). Similarly, in guinea pig gastric antrum myocytes, SNP increases intermediate-conductance K Ca current and enhances STOCs, which are sensitive to inositol (1,4,5)-trisphosphate receptor (IP 3 R) inhibitors (58). These findings suggest that sarcoplasmic reticulum (SR) Ca 2ϩ release plays a role in the nitrergic relaxation of smooth muscles.In several smooth muscles...

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Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Cited by 89 publications

References 707 publications

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries

CaM kinase II activation and phospholamban phosphorylation by SNP in murine gastric antrum smooth muscles

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Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Cited by 89 publications

References 707 publications

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

Ca2+ entry following P2X receptor activation induces IP3 receptor‐mediated Ca2+ release in myocytes from small renal arteries

CaM kinase II activation and phospholamban phosphorylation by SNP in murine gastric antrum smooth muscles

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Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries