Analysis of hyperpolarizing afterpotentials in the atrial myocardium.
Afterpotentials following a train of paced action potentials in isolated pectinate muscles bordering the crista terminalis in the rabbit atrial myocardium were analyzed. Electrical measurements were performed using a standard microelectrode technique. An ultrastructural stereological analysis was undertaken to study intercellular clefts within the preparations used. After cessation of a rapid drive, afterpotentials showed an initial depolarization followed by a delayed hyperpolarization. The initial depolarization could be blocked by verapamil (13.2 microM) leaving a monotonous hyperpolarization. This hyperpolarization was modelled supposing a K+-depletion out of morphological identified intercellular clefts. From best approximation of the measured after-hyperpolarization (1) the internal K+ activity was estimated to be in the range of 82 to 90 mM depending on the pacing interval Io. It decreased due to shortening of Io; (2) the accumulated "cleft" K+ activity was estimated to be about 2 mM at a pre-drive pacing interval of 250 ms; it decreased by increasing of Io, (3) decreasing of Io accelerated the K+-depletion, (4) a single beat accumulation of about 0.28 mM was estimated. The morphologically measured geometry of the intercellular clefts (mean cleft width 0.5 micron, ratio of cleft and cell volume 0.09 +/- 0.03) agreed well with the electrophysiological findings.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D016275:Atrial Function; D004594:Electrophysiology; D006321:Heart / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D014700:Verapamil; D011188:Potassium