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Activation of muscarinic K+ current in guinea‐pig atrial myocytes by a serum factor.

1. Atrial myocytes obtained by enzymatic perfusion of hearts from adult guinea‐pigs and cultured for 0‐14 days were studied using the whole‐cell voltage‐clamp technique. 2. Superfusion of the myocytes with diluted sera (1:100 to 1:10,000) from different species (human, horse, guinea‐pig) evoked an inward rectifying K+ current. The voltage‐dependent properties of this current were identical to those of the K+ current activated by acetylcholine (IK(ACh)). Current density in the presence of horse serum (1:100) approximately corresponded to the non‐desensitizing fraction of IK(ACh) during superfusion with 1‐2 x 10(‐6) M ACh. 3. During a maximal serum‐evoked current, application of ACh (10(‐6) M) failed to evoke additional K+ current. After switching superfusion from serum‐containing to serum‐free solution, the K+ current decayed 1‐2 orders of magnitude slower than ACh‐activated IK(ACh). During the decay of the serum‐evoked current, a proportional increase in responsiveness to ACh was recorded. During submaximal activation of K+ current by serum, a saturating concentration of ACh resulted in a total current that was identical to the current evoked by ACh alone minus the desensitizing component. Thus, activation of K+ current by serum caused desensitization of IK(ACh). From these results it is concluded that sera contain a factor that activates the same population of K+ channels as ACh. 4. Irreversible activation of IK(ACh) by ACh in myocytes dialysed with the GTP‐analogue GTP‐gamma‐S abolished sensitivity to serum and vice versa. 5. The effect of serum was not modified by atropine (10(‐6) M) which completely blocked the response to 2 x 10(‐6) M ACh. Furthermore, theophylline (1 mM), which completely inhibited IK(ACh) activation by adenosine (100 microM), failed to inhibit the effect of serum. Thus, neither muscarinic nor purinergic (A1) receptors are involved. 6. The peptide somatostatin (10(‐6) M) and the alpha 1‐agonist phenylephrine (1 microM) which previously have been shown to cause activation of IK(ACh) channels, in the present study failed to evoke any measurable current, which excludes the involvement of the corresponding receptors. 7. Pre‐incubation of the cells with pertussis toxin completely abolished IK(ACh) evoked by ACh, adenosine and serum, suggesting that the activating factor, like the classical agonists, causes opening of IK(ACh) channels via a G protein (Gi, GK). 8. The potency of serum to activate IK(ACh) was not reduced by dialysis, suggesting the molecular mass of the unknown factor to be > or = 5 kDa. No activating potency was found in the dialysing solutions.(ABSTRACT TRUNCATED AT 400 WORDS)