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Article: Regulation of vascular tone: cross-talk between sarcoplasmic reticulum and plasmalemma

TitleRegulation of vascular tone: cross-talk between sarcoplasmic reticulum and plasmalemma
Authors
Keywordscalcium channels
calcium pumps
endothelial cell
plasma membranes
sarcoplasmic reticulum
vascular smooth muscle
Issue Date1995
PublisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
Citation
Canadian Journal of Physiology and Pharmacology, 1995, v. 73 n. 5, p. 551-557 How to Cite?
AbstractSelected topics on the roles of sarcoplasmic reticulum (SR) in the control of vascular smooth muscle (VSM) tone are briefly reviewed with particular reference to the regulation of cytosolic concentration of free calcium ions, [Ca2+]i. Although morphological evidence and subcellular membrane studies indicate a relatively meager quantity of SR in VSM and of endoplasmic reticulum (ER) in endothelial cells (ECs) compared with skeletal muscle and cardiac muscle, contractility studies suggest that vascular tone is, to a large extent, regulated by the intracellular Ca2+ stores in smooth muscle and endothelial cells. Cytosolic Ca2+ levels control myosin light chain phosphorylation and contraction in VSM and activation of NO synthase and phospholipase A2 in ECs to regulate nitric oxide (NO) and prostaglandin I2 formation. Understanding of the importance of SR or ER in modulating the [Ca2+]i in VSM and ECs has been further advanced as a result of the new development and refinement of biophysical techniques in the measurement of cellular Ca2+ concentrations and ion currents, such as fluorescent Ca2+ indicators and patch-clamp techniques. Experimental evidence has accumulated in support of the existence of cross-talk between SR-ER and the plasma membrane (PM). Novel pharmacological tool drugs selective for the SR-ER Ca2+ pump, such as thapsigargin and cyclopiazonic acid, as well as for SR-ER Ca2+ channels, such as ryanodine (for the Ca(2+)-induced Ca2+ release channel) and inositol polyphosphates and heparin (for the inositol-1,4,5-trisphosphate activated Ca2+ channel), together with the use of blockers for selective PM Ca2+ channels have enabled better formulation and elucidation of the mechanisms of cross-talk between SR-ER and PM.(ABSTRACT TRUNCATED AT 250 WORDS)
Persistent Identifierhttp://hdl.handle.net/10722/43479
ISSN
2023 Impact Factor: 1.7
2023 SCImago Journal Rankings: 0.499
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDaniel, EEen_HK
dc.contributor.authorVan Breemen, Cen_HK
dc.contributor.authorSchilling, WPen_HK
dc.contributor.authorKwan, CYen_HK
dc.date.accessioned2007-03-23T04:46:32Z-
dc.date.available2007-03-23T04:46:32Z-
dc.date.issued1995en_HK
dc.identifier.citationCanadian Journal of Physiology and Pharmacology, 1995, v. 73 n. 5, p. 551-557en_HK
dc.identifier.issn0008-4212en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43479-
dc.description.abstractSelected topics on the roles of sarcoplasmic reticulum (SR) in the control of vascular smooth muscle (VSM) tone are briefly reviewed with particular reference to the regulation of cytosolic concentration of free calcium ions, [Ca2+]i. Although morphological evidence and subcellular membrane studies indicate a relatively meager quantity of SR in VSM and of endoplasmic reticulum (ER) in endothelial cells (ECs) compared with skeletal muscle and cardiac muscle, contractility studies suggest that vascular tone is, to a large extent, regulated by the intracellular Ca2+ stores in smooth muscle and endothelial cells. Cytosolic Ca2+ levels control myosin light chain phosphorylation and contraction in VSM and activation of NO synthase and phospholipase A2 in ECs to regulate nitric oxide (NO) and prostaglandin I2 formation. Understanding of the importance of SR or ER in modulating the [Ca2+]i in VSM and ECs has been further advanced as a result of the new development and refinement of biophysical techniques in the measurement of cellular Ca2+ concentrations and ion currents, such as fluorescent Ca2+ indicators and patch-clamp techniques. Experimental evidence has accumulated in support of the existence of cross-talk between SR-ER and the plasma membrane (PM). Novel pharmacological tool drugs selective for the SR-ER Ca2+ pump, such as thapsigargin and cyclopiazonic acid, as well as for SR-ER Ca2+ channels, such as ryanodine (for the Ca(2+)-induced Ca2+ release channel) and inositol polyphosphates and heparin (for the inositol-1,4,5-trisphosphate activated Ca2+ channel), together with the use of blockers for selective PM Ca2+ channels have enabled better formulation and elucidation of the mechanisms of cross-talk between SR-ER and PM.(ABSTRACT TRUNCATED AT 250 WORDS)en_HK
dc.format.extent1430541 bytes-
dc.format.extent25600 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjppen_HK
dc.rightsCanadian Journal of Physiology and Pharmacology. Copyright © N R C Research Press.en_HK
dc.subjectcalcium channels-
dc.subjectcalcium pumps-
dc.subjectendothelial cell-
dc.subjectplasma membranes-
dc.subjectsarcoplasmic reticulum-
dc.subjectvascular smooth muscle-
dc.subject.meshBlood vessels - physiologyen_HK
dc.subject.meshCalcium - physiologyen_HK
dc.subject.meshMuscle, smooth, vascular - physiologyen_HK
dc.subject.meshSarcoplasmic reticulum - physiologyen_HK
dc.subject.meshCalcium channels - physiologyen_HK
dc.titleRegulation of vascular tone: cross-talk between sarcoplasmic reticulum and plasmalemmaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-4212&volume=73&issue=5&spage=551&epage=557&date=1995&atitle=Regulation+of+vascular+tone:+cross-talk+between+sarcoplasmic+reticulum+and+plasmalemmaen_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1139/y95-070-
dc.identifier.pmid7585320-
dc.identifier.scopuseid_2-s2.0-0029115673-
dc.identifier.hkuros11246-
dc.identifier.isiWOS:A1995RL90700005-
dc.identifier.issnl0008-4212-

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