Ca2+ microdomains in smooth muscle

McCarron, John G.; Chalmers, Susan; Bradley, Karen N.; MacMillan, Debbi; Muir, T. C.

doi:10.1016/j.ceca.2006.08.010

Cited by 86 publications

(70 citation statements)

References 411 publications

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“…The resolution of this paradox has been suggested to lie in the local control of Ca 2+ microdomains that function and are regulated autonomously (Berridge, 1997), the gradual recruitment of which by gradually increasing stimuli would result in graded Ca 2+ signals. Imaging microdomain Ca 2+ in muscle cells has reshaped our understanding of Ca 2+ signalling and provided direct evidence to validate the local control theory in skeletal, cardiac and smooth muscles (Wang et al, 2004;McCarron et al, 2006).In smooth muscles, IP3R-mediated Ca 2+ release is essential for [Ca 2+ ]i mobilization and contraction, especially (but not exclusively) induced by stimulation with neurotransmitters and hormones (Boittin et al, 1999;Bayguinov et al, 2000;McCarron et al, 2002;Zhang et al, 2003;Lamont and Wier, 2004;MacMillan et al, 2005;Gordienko et al, 2008). The role of IP3Rs seems to be to facilitate CICR within and between RyRs domains (Boittin et al, 1998;Gordienko and Bolton, 2002;White and McGeown, 2002;Zhang et al, 2003).…”

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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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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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“…caffeine), by Ca 2+ influx from outside the cell in the process of Ca 2+ -induced Ca 2+ release (CICR), or when the stores's Ca 2+ content exceeds normal physiological values, i.e. in 'store overload' [2][3][4][5][6]. Activation of either receptor allows diffusion of Ca 2+ from the store to increase the cytoplasmic Ca 2+ concentration ([Ca 2+ ] c ) from the resting value of ~100 nM to ~1 μM for many seconds throughout the cell and briefly (e.g.…”

Section: Introductionmentioning

confidence: 99%

Calcium Mobilization via Intracellular Ion Channels, Store Organization and Mitochondria in Smooth Muscle

McCarron

Chalmers

Wilson

et al. 2016

Vascular Ion Channels in Physiology and Disease

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This version is available at https://strathprints.strath.ac.uk/55095/ Strathprints is designed to allow users to access the research output of the University of Strathclyde. Unless otherwise explicitly stated on the manuscript, Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Please check the manuscript for details of any other licences that may have been applied. You may not engage in further distribution of the material for any profitmaking activities or any commercial gain. You may freely distribute both the url (https://strathprints.strath.ac.uk/) and the content of this paper for research or private study, educational, or not-for-profit purposes without prior permission or charge.Any correspondence concerning this service should be sent to the Strathprints administrator: strathprints@strath.ac.ukThe Strathprints institutional repository (https://strathprints.strath.ac.uk) is a digital archive of University of Strathclyde research outputs. It has been developed to disseminate open access research outputs, expose data about those outputs, and enable the management and persistent access to Strathclyde's intellectual output. Abstract In smooth muscle, Ca 2+ release from the internal store into the cytoplasm occurs via inositol trisphosphate (IP 3 R) and ryanodine receptors (RyR). The internal Ca 2+ stores containing IP 3 R and RyR may be arranged as multiple separate compartments with various IP 3 R and RyR arrangements, or there may be a single structure containing both receptors. The existence of multiple stores is proposed to explain several physiological responses which include the progression of Ca 2+ waves, graded Ca 2+ release from the store and various local responses and sensitivities. We suggest that, rather than multiple stores, a single luminally-continuous store exists in which Ca 2+ is in free diffusional equilibrium throughout. Regulation of Ca 2+ release via IP 3 R and RyR by the local Ca 2+ concentration within the stores explains the apparent existence of multiple stores and physiological processes such as graded Ca 2+ release and Ca 2+ waves. Close positioning of IP 3 R on the store with mitochondria or with receptors on the plasma membrane creates 'IP 3 junctions' to generate local responses on the luminally-continuous store.

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“…The (Somlyo & Somlyo, 1994;Gollasch et al, 2000;McCarron et al, 2006). [Ca 2+ ] i levels are modulated by either influx/efflux across the plasmalemma and or release/sequestration into intracellular calcium stores predominantly, but not exclusively, the sarcoplasmic reticulum (SR).…”

Section: Mechanisms Controlling Arterial Contractility; Role Of Intramentioning

confidence: 99%

“…(Although a brief overview of the main mechanisms is given below a detailed discussion of the mechanisms which modulate calcium homeostasis in smooth muscle is beyond the scope of this text and as such we direct the reader towards reviews of this area for more information (Amberg & Navedo, 2013;Hill-Eubanks et al, 2011;Kudryavtseva et al, 2013)). The relationship between Ca 2+ and contraction is, however, not straightforward and it is now evident that subcellular Ca 2+ fluxes and microdomains exist which may differentially modulate contractile function (Gollasch et al, 2000;McCarron et al, 2006). Whilst an increase in global [Ca 2+ ] i promotes arterial contraction, localised increases in Ca 2+ may have different effects on contraction.…”

Section: Mechanisms Controlling Arterial Contractility; Role Of Intramentioning

confidence: 99%

Plasma membrane calcium ATPases (PMCAs) as potential targets for the treatment of essential hypertension

Little

Cartwright

Neyses

et al. 2016

Pharmacology & Therapeutics

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The incidence of hypertension, the major modifiable risk factor for cardiovascular disease, is increasing. Thus, there is a pressing need for the development of new and more effective strategies to prevent and treat hypertension. Development of these relies on a continued evolution of our understanding of the mechanisms which control blood pressure (BP). Resistance arteries are important in the regulation of total peripheral resistance and BP; changes in their structure and function are strongly associated with hypertension. Anti-hypertensives which both reduce BP and reverse changes in resistance arterial structure reduce cardiovascular risk more than therapies which reduce BP alone. Hence, identification of novel potential vascular targets which modify BP is important. Hypertension is a multifactorial disorder which may include a genetic component. Genome wide association studies have identified ATP2B1, encoding the calcium pump plasma membrane calcium ATPase 1 (PMCA1), as having a strong association with BP and hypertension. Knockdown or reduced PMCA1 expression in mice has confirmed a physiological role for PMCA1 in BP and resistance arterial regulation. Altered expression or inhibition of PMCA4 has also been shown to modulate these parameters. The mechanisms whereby PMCA1 and 4 can modulate vascular function remain to be fully elucidated but may involve regulation of intracellular calcium homeostasis and/or comprise a structural role. However, clear physiological links between PMCA and BP, coupled with experimental studies directly linking PMCA1 and 4 to changes in BP and arterial function, suggest that they may be important targets for the development of new pharmacological modulators of BP.

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Ca2+ microdomains in smooth muscle

Cited by 86 publications

References 411 publications

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

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

Calcium Mobilization via Intracellular Ion Channels, Store Organization and Mitochondria in Smooth Muscle

Plasma membrane calcium ATPases (PMCAs) as potential targets for the treatment of essential hypertension

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Ca2+ microdomains in smooth muscle

Cited by 86 publications

References 411 publications

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

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

Calcium Mobilization via Intracellular Ion Channels, Store Organization and Mitochondria in Smooth Muscle

Plasma membrane calcium ATPases (PMCAs) as potential targets for the treatment of essential hypertension

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

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