title: Preceding stimulus frequency-dependent potentiation of the postrest shortening of the action potential duration in rabbits.
abstract: Action potential duration (APD) in rabbit ventricular myocardium shortens after a rest period (postrest shortening). However, the effects of preceding stimulus frequency on the postrest shortening have not been elucidated. We recorded transmembrane action potentials (TAPs) and monophasic action potentials (MAPs) from the rabbit ventricle. In in vitro experiments. repetitive regular stimuli (S1) at cycle lengths ranging between 500 to 3000 ms were followed by a single extrastimulus (S2) at a coupling interval of 5000 ms. A decrease in S1S1 interval resulted in a progressive shortening of the duration of TAP (TAPD) elicited by S2 (S2-TAPD), which was potentiated by increasing extracellular calcium concentration ([Ca2+]o) or application of ouabain and was inhibited by lowering [Ca2+]o or verapamil. Application of ryanodine was most effective in lengthening S2-TAPD following a short S1S1 interval. 4-aminopyridine and E4031 caused marked lengthening of S2-TAPD when S1S1 was long. However, the lengthening effect was attenuated and disappeared with a shorter S1S1 interval. In in vivo experiments, regular ventricular pacing (S1) at cycle lengths ranging between 250 to 1000 ms was followed by a single extrastimulus (S2) with a coupling interval (S1S2) of 1500 ms. A decrease in the S1S1 interval also resulted in progressive shortening of the duration of MAP elicited by S2. Our results indicate that the postrest shortening is potentiated by an increase in the preceding stimulus frequency in the rabbit ventricle, in which the function of sarcoplasmic reticulum may play a significant role.
authors.affiliation: Department of Internal Medicine I, School of Medicine, Oita Medical University, Hasama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Takahashi
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: S
authors.initials: S
authors.lastname: Ishida
authors.forename: T
authors.initials: T
authors.lastname: Fujino
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: H
authors.initials: H
authors.lastname: Yonemochi
authors.forename: T
authors.initials: T
authors.lastname: Iwao
authors.forename: T
authors.initials: T
authors.lastname: Ooie
authors.forename: M
authors.initials: M
authors.lastname: Hara
authors.forename: T
authors.initials: T
authors.lastname: Saikawa
authors.forename: T
authors.initials: T
authors.lastname: Sakata
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D004558:Electric Stimulation; D004562:Electrocardiography; D004594:Electrophysiology; D066298:In Vitro Techniques; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D010210:Papillary Muscles / Q000502:physiology; D026902:Potassium Channel Blockers; D011817:Rabbits; D012146:Rest; D012433:Ryanodine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000502:physiology; D016276:Ventricular Function / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology
chemical_list: D026902:Potassium Channel Blockers; D012433:Ryanodine; D010042:Ouabain; D014700:Verapamil; D002118:Calcium