摘要：

Adenosine decreases the force of contraction in atrial muscle, the uptake of Ca2+, the plateau phase and duration of the action potential. In contrast to acetylcholine which increases K+ permeability the effects of adenosine are antagonized by caffeine and are not blocked by atropine. It has been suggested that these effects of adenosine are mediated by a depression of the cell membrane to Ca2+ permeability. In order to test this hypothesis we attempted to determine whether adenosine had inhibitory effects on the slow action potential of potassium-depolarized (20 mm) atrial muscle treated with norepinephrine (5 × 105m). With the slow action potentials it appears that Ca2+ carries the inward current since (1) the overshoot varies according to the Nernst equation upon changes in extracellular [Ca2+], (2) changes in inward ionic flow associated with the action potential are paralleled by changes in developed tension. Adenosine at micromolar concentrations reduced within seconds the rate of rise and amplitude of the action potential. The action potentials lost their all-or-none nature and appeared graded with adenosine. The muscle became completely inexcitable at concentrations as low as 10.2 μm. These effects of adenosine could either be reversed within seconds by enzymatic degradation of adenosine or by raising the extracellular [Ca2+]. These findings suggest that adenosine depresses the membrane permeability to Ca2+ either directly or through an indirect membrane stabilizing effect mediated by permeability changes in Na+ or K+ ions. This effect of adenosine possibly occurs on the extracellular side of the membrane since adenosine can only exist extracellularly and large and charged adenosine derivatives (ATP, ADP, AMP, c-AMP, NAD and NADP) that probably do not penetrate the cell cause similar effects.

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