Computational model of the ventricular action potential in adult spontaneously hypertensive rats

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dc.contributor.authorPadmala, Srikanthen_US
dc.contributor.authorDemir, Sıddıka Semahaten_US
dc.date.accessioned2019-08-31T12:10:23Z
dc.date.accessioned2019-08-05T16:05:06Z
dc.date.available2019-08-31T12:10:23Z
dc.date.available2019-08-05T16:05:06Z
dc.date.issued2003-09-01
dc.departmentIşık Üniversitesi, Mühendislik Fakültesi, Biyomedikal Mühendisliği Bölümüen_US
dc.departmentIşık University, Faculty of Engineering, Department of Biomedical Engineeringen_US
dc.description.abstractIntroduction: Cardiac hypertrophy has substantial clinical significance because many hypertrophic cells have markedly prolonged repolarization behavior, which may lead to increased risk for cardiac arrhythmias. Spontaneously hypertensive rat (SHR) is one model of hypertension that is studied extensively and is considered to be the best laboratory model of human hypertension. We extended our previously published model of the rat ventricular myocyte to simulate the effects of hypertrophy in SHR. Methods and Results: In SHR it has been shown that the membrane capacitance is increased, the density of transient outward K+ current is decreased, the sarcoplasmic reticulum Ca 2+ ATPase activity is reduced, and the cell volumes are increased compared to those of the normal rat. We introduced these changes into our previous model of the rat ventricular myocyte and simulated the ventricular action potential of SHR. Our results demonstrated increased action potential duration (APD) and increased peak systolic value of the intracellular calcium transient in SHR. Simulations with reduced extracellular K+ concentration ([K+]o) have shown that there is increased APD shortening in SHR compared to that of the normal rat. Conclusions: Our computational model qualitatively simulated the electrophysiologic changes observed in SHR and provided the plausible mechanistic linkage between the prolonged APD and increased inotropy. Our model results also demonstrated the electrophysiologic changes observed with reduced [K+]o in SHR, a finding that is clinically significant in hypertensive patients with left ventricular hypertrophy undergoing diuretic treatment.en_US
dc.description.versionPublisher's Versionen_US
dc.identifier.citationPadmala, S. & Demir, S. S. (2003). Computational model of the ventricular action potential in adult spontaneously hypertensive rats.Journal of Cardiovascular Electrophysiology. 14(9), 990-995. doi:10.1046/j.1540-8167.2003.03086.xen_US
dc.identifier.doi10.1046/j.1540-8167.2003.03086.x
dc.identifier.endpage995
dc.identifier.issn1045-3873
dc.identifier.issue9
dc.identifier.pmid12950545
dc.identifier.scopus2-s2.0-0141724661
dc.identifier.scopusqualityQ1
dc.identifier.startpage990
dc.identifier.urihttps://hdl.handle.net/11729/2053
dc.identifier.urihttps://dx.doi.org/10.1046/j.1540-8167.2003.03086.x
dc.identifier.volume14
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorDemir, Sıddıka Semahaten_US
dc.language.isoenen_US
dc.peerreviewedYesen_US
dc.publicationstatusPublisheden_US
dc.relation.ispartofJournal of Cardiovascular Electrophysiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAction potential durationen_US
dc.subjectAction potentialen_US
dc.subjectAction potentialsen_US
dc.subjectAdenosine triphosphatase (calcium)en_US
dc.subjectAdulthooden_US
dc.subjectAnimalen_US
dc.subjectAnimalsen_US
dc.subjectArticleen_US
dc.subjectBiological modelen_US
dc.subjectCalciumen_US
dc.subjectCalcium cell levelen_US
dc.subjectCalcium transienten_US
dc.subjectCalcium transporten_US
dc.subjectCardiac myocyteen_US
dc.subjectCell volumeen_US
dc.subjectComputational modelen_US
dc.subjectElectric capacitanceen_US
dc.subjectEnzyme activityen_US
dc.subjectEnzyme assayen_US
dc.subjectExtracellular fluiden_US
dc.subjectHeart electrophysiologyen_US
dc.subjectHeart muscle cellen_US
dc.subjectHeart muscle potentialen_US
dc.subjectHeart ventricleen_US
dc.subjectHeart ventricle functionen_US
dc.subjectHeart ventricle hypertrophyen_US
dc.subjectHeart ventriclesen_US
dc.subjectHypertensen_US
dc.subjectHypertensionen_US
dc.subjectHypertrophyen_US
dc.subjectIntracellular membraneen_US
dc.subjectIntracellular membranesen_US
dc.subjectIon channelen_US
dc.subjectIon channelsen_US
dc.subjectIoninotropismen_US
dc.subjectKv channel-interacting proteinsen_US
dc.subjectMathematical modelen_US
dc.subjectMetabolismen_US
dc.subjectModels, Cardiovascularen_US
dc.subjectMyocytes, Cardiacen_US
dc.subjectOsmolar concentrationen_US
dc.subjectOsmolarityen_US
dc.subjectPathophysiologyen_US
dc.subjectPotassiumen_US
dc.subjectPotassium channelsen_US
dc.subjectPotassium currenten_US
dc.subjectPotassium ionen_US
dc.subjectPriority journalen_US
dc.subjectQualitative analysisen_US
dc.subjectRaten_US
dc.subjectRatsen_US
dc.subjectRats, Inbred SHRen_US
dc.subjectReaction timeen_US
dc.subjectSarcoplasmic reticulumen_US
dc.subjectSimulationen_US
dc.subjectSpontaneously hypertensive ratsen_US
dc.subjectSpontaneously hypertensive raten_US
dc.subjectSystoleen_US
dc.subjectTransient outwarden_US
dc.subjectVentricular functionen_US
dc.subjectVoltage-gateden_US
dc.titleComputational model of the ventricular action potential in adult spontaneously hypertensive ratsen_US
dc.typeArticleen_US
dspace.entity.typePublication

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