Effects of extracellular potassium on slow response excitability in rabbit atrial trabeculae.

Abstract

Small trabeculae were excised from the rabbit left atrium and exposed to 1 mmol . litre-1 Ba2+-Tyrode solution containing variable amounts of potassium (range: 10 to 25 mmol . litre-1). One end of the trabecula was stimulated by means of a suction electrode. Intracellular microelectrodes were employed for measuring membrane potentials. In presence of Ba2+, the cell depolarises and slow responses can be elicited. Slow responses thus obtained do not propagate. Slow response overshoot, maximum rate of rise and duration are depressed by increasing extracellular potassium concentrations ([K+]o). The resting potential decreases by 1 to 3 mV on changing [K+]o from 10 to 25 mmol . litre-1. The depression in slow response overshoot caused by [K+]o is compatible with an increase in the relationship between K+ and Ca2+ permeabilities as [K+]o increases. The dependence of slow response excitability on the frequency of stimulation is also depressed by [K+]o. The inhibition of slow response electrogenesis caused by extracellular potassium is an important phenomenon to consider in trying to understand the origin of certain cardiac arrhythmias.