dc.creatorLascano, Elena C.
dc.creatorNegroni, Jorge A.
dc.date2006-03
dc.date2022-12-07T13:24:18Z
dc.date.accessioned2023-07-15T09:03:19Z
dc.date.available2023-07-15T09:03:19Z
dc.identifierhttp://sedici.unlp.edu.ar/handle/10915/146976
dc.identifierhttps://pmr.safisiol.org.ar/wp-content/uploads/2022/09/vol1_n8_march.pdf
dc.identifierissn:1669-5410
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/7486648
dc.descriptionIn the normoperfused heart, Ca²⁺ enters the myocardial cell through voltagedependent Ca²⁺ channels and is extruded through the sarcolemmal Ca²⁺ pump and the Na+/Ca²⁺ exchanger. During ischemia and early reperfusion, however, sarcoplasmic reticulum reuptake and sarcolemmal Ca²⁺ pump activities are impaired due to decreased ATP. In addition, owing to defective Na⁺-K⁺ pump performance and low pH favoring Na⁺ entry in exchange for H⁺ output through the Na⁺/H⁺ exchanger, the Na⁺/Ca²⁺ exchanger operates in its reverse mode incorporating Ca²⁺ to diminish increased intracellular Na⁺. Thus, the resulting impaired Ca²⁺ balance produces Ca²⁺ overload and myocardial injury probably by activation of Ca²⁺-dependent proteases which can partially destroy contractile proteins leading to decreased responsiveness of contractile filaments to Ca²⁺ (18). This chain of ischemic events is in part counteracted by activation of ATP-dependent K⁺ (KATP) channels which by allowing earlier passive K⁺ output, shortens action potential duration and reduces the time during which Ca²⁺ can enter the cell.
dc.descriptionSociedad Argentina de Fisiología
dc.formatapplication/pdf
dc.languagees
dc.rightshttp://creativecommons.org/licenses/by/4.0/
dc.rightsCreative Commons Attribution 4.0 International (CC BY 4.0)
dc.subjectCiencias Médicas
dc.subjectFisiología
dc.subjectIschemia
dc.subjectPotassium
dc.titleRole of sarcolemmal ATP-dependent K⁺ channels in cardiac ischemic injury
dc.typeArticulo
dc.typeRevision


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