OVERDRIVE EXCITATION IN THE GUINEA-PIG SINOATRIAL NODE SUPERFUSED IN HIGH [K+](O)

Citation
Y. Choy et al., OVERDRIVE EXCITATION IN THE GUINEA-PIG SINOATRIAL NODE SUPERFUSED IN HIGH [K+](O), Journal of biomedical science, 4(4), 1997, pp. 179-191
Citations number
34
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
10217770
Volume
4
Issue
4
Year of publication
1997
Pages
179 - 191
Database
ISI
SICI code
1021-7770(1997)4:4<179:OEITGS>2.0.ZU;2-#
Abstract
The aim of the present experiments was to study the characteristics an d mechanisms of the rhythm induced by overdrive ('overdrive excitation ', OBE) in the sinoatrial node (SAN) superfused in high [K+](0) (8-14 mM). It was found that: (I)overdrive may induce excitation in quiescen t SAN and during a slow drive; (2) in spontaneously active SAN, overdr ive may accelerate the spontaneous discharge; (3) immediately after th e end of overdrive, a pause generally precedes the onset of the induce d rhythm; (4) during the pause, an oscillatory potential (V-os) may be superimposed on the early diastolic depolarization (DD); (5) during t he subsequent late DD, a different kind of oscillatory potential appea rs near the threshold for the upstroke (ThVos) which is responsible fo r the initiation of spontaneous activity; (6) once started, the induce d rhythm is fastest soon after overdrive; (7) faster drives induce lon ger and faster spontaneous rhythms; (8) the induced action potentials are slow responses followed by DD with a superimposed V-os, but ThVos is responsible for ODE; (9) the induced rhythm subsides when ThVos mis s the threshold and gradually decay; (10) low [Ca2+](o) abolishes ODE; (11) in quiescent SAN, high [Ca2+](o) induces spontaneous discharge t hrough ThVos and increases its rate by enhancing V-os and shifting the threshold to more negative values, and(12)tetrodotoxin abolishes ODE as well as the spontaneous discharge induced by high [Ca2+](o). In con clusion, in K+-depolarized SAN, ODE may be present in the apparent abs ence of calcium overload, is Ca2+- and Na+-dependent and is mediated b y ThVos and not by V-os.