title: Post-partum prolongation of the atrial repolarization in rabbit.
abstract: Female sexual steroids are known to modify the expression of various K+ channels and thus they can alter cardiac repolarization. In the present work, using conventional microelectrode techniques, action potential characteristics were studied in atrial myocardium isolated from virgin, late pregnant, early (1-3 days) post-partum and late (2-3 weeks) post-partum rabbits. No changes in action potential configuration were observed during pregnancy. However, the duration, overshoot and amplitude of action potentials were significantly increased in the early (1-3 days) post-partum period. Resting potential and maximum rate of depolarization remained unchanged. The observed changes were transient, normal action potential characteristics were obtained at weeks 2-3 post-partum. 4-aminopyridine (1 mmol L(-1)). caused a marked lengthening of action potential duration in all preparations obtained from non-pregnant and pregnant rabbits, whereas this 4-aminopyridine-induced prolongation was moderate in those preparations excised from the hearts of early post-partum animals. Action potential configuration was not affected by pinacidil (10 micromol L(-1)) or glibenclamide (5 micromol L(-1)) in non-pregnant or pregnant animals. In preparations obtained from early post-partum rabbits, pinacidil significantly shortened action potential duration, which was reverted by glibenclamide. The lengthening of action potential duration together with the decreased sensitivity to 4-aminopyridine observed in early post-partum animals may probably be caused by reduction of the transient outward K+ current at this stage. The results also suggest that electrophysiological alterations in the early post-partum period may probably be more pronounced than those associated with pregnancy itself.
authors.affiliation: Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: P
authors.initials: P
authors.lastname: Pacher
authors.forename: Z
authors.initials: Z
authors.lastname: Ungvári
authors.forename: P P
authors.initials: PP
authors.lastname: Nánási
authors.forename: I
authors.initials: I
authors.lastname: Mucha
authors.forename: V
authors.initials: V
authors.lastname: Kecskeméti
authors.forename: G
authors.initials: G
authors.lastname: Losonczy
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D016275:Atrial Function; D004594:Electrophysiology; D004967:Estrogens / Q000502:physiology; D005260:Female; D005905:Glyburide / Q000494:pharmacology; D006325:Heart Atria / Q000166:cytology; D006329:Heart Conduction System / Q000502:physiology*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D018485:Muscle Fibers, Skeletal / Q000737:chemistry / Q000502:physiology; D009206:Myocardium / Q000737:chemistry / Q000166:cytology*; D020110:Pinacidil / Q000494:pharmacology; D049590:Postpartum Period / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D011247:Pregnancy; D011817:Rabbits; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004967:Estrogens; D007004:Hypoglycemic Agents; D015221:Potassium Channels; D014665:Vasodilator Agents; D020110:Pinacidil; D015761:4-Aminopyridine; D005905:Glyburide