.BETA.-Actions of catecholamines on the K-related currents of the bullfrog atrial muscle.

Abstract

Effects of catecholamines on K-related membrane currents in the bullfrog atrial muscle were studied under voltage clamp using the double sucrose-gap technique. Isoproterenol (10-8l0_6 M) and norepinephrine (5 x 10-6-10-5 M) induced an outward shift of the basal current level and enhanced both the background current (Ib) for hyperpolarization and the instantaneous outward current for depolarization. There was an augmentation of the slow inward current (Isi) and the delayed outward current (Ij.The augmentation of I, was induced with or without an increase in Isi, but different kinetics were involved. In the presence of Isi, j3-agonists produced a more marked augmentation of I, for the intermediate voltages of depolarization where Isi was enhanced, and Co eliminated these effects. In the absence of Isi with Co, j3-agonists elicited an enhancement of Ig; however, the enhancement was greater for larger and longer depolarizations. All these effects were absent in the presence of propranolol (5 x 10-7 M). These observations indicate that j3-agonists directly increase the background K current, and enhance the delayed outward current (Is) via two different mechanisms; one is related to the augmentation of Isi and the other is not.

Modulation of the delayed rectifier potassium current in frog cardiomyocytes by beta‐adrenergic agonists and magnesium.

“…1A) (Falk & Cohen, 1984;Desilets & Baumgarten, 1988;Shah, Cohen & Rosen, 1988) (Isenberg, 1977a, b;Goto, Hyodo & Ikeda, 1983) that contaminates IK. In support of this suggestion is the finding that blocking 1Ca with D600 blocks the effect of adrenaline on IK in rabbit sino-atrial node (Brown & DiFrancesco, 1980) and that 1 mM-Co2+ reduces the effects of fl-agonists on IK at voltages in the range where ICa is activated (Umeno, 1984). To test these alternative possibilities, Hume (1985) examined the effects of fl-agonists on IK in isolated frog atrial cells, and found that ,8-agonists had no effect on IK even when 'Ca increased severalfold.…”

“…We use a system that dialyses the cell interior, whereas Hume used relatively high-resistance pipettes. One could argue that the cell responds to fl-adrenergic agonists only after it has been internally perfused, but this seems unlikely since Brown & Noble (1974) and Umeno (1984) both find fl-adrenergicinduced increases in IK in multicellular preparations of frog atrium. One wonders whether adrenaline, which was used by Hume, might affect both a-and fl-receptors and that a-receptor activation might have opposite effects to fl-receptor activation (Handa, Wagner, Inui, Averesch & Schumann, 1982) or whether the enzymatic dissociation procedure altered the coupling between fl-receptors and IK in some interesting way.…”

“…Studies on both multicellular preparations and isolated cells have demonstrated that /I-adrenergic agonists increase the amplitude of IK (Tsien, Giles & Greengard, 1972;Brown & Noble, 1974;Brown, DiFrancesco & Noble, 1979;Pappano & Carmeliet, 1979;Brown & DiFrancesco, 1980;Noma, Kotake & Irisawa, 1980; Kass & Weigers, 1982; Osterrieder, Brum, Hescheler, Trautwein, Flockerzi & Hofmann, 1982;Brum, Flockerzi, Hofmann, Osterrieder & Trautwein, 1983;Umeno, 1984; Kameyama, Hofmann & Trautwein, 1985; Kameyama, Hescheler, Hofmann & Trautwein, 1986; Bennett, McKinney, Begenisich & Kass, 1986;Carmeliet & Mubagwa, 1986;Bennett & Begenisich, 1987;Walsh, Begenisich & Kass, 1988;. It has been suggested, however, that this apparent increase inIK is at least partly an artifact resulting from stimulation of ICa and subsequent activation of Ca2+_ dependent K+ conductances or stimulation of the Na+-K+ pump resulting in changes in K+ driving force (Brown et al 1979;Umeno, 1984;Hume, 1985).…”

Modulation of the delayed rectifier K+ current by isoprenaline in bull‐frog atrial myocytes.

“…No negative shift in EK was observed; hence an increase in electrochemical driving force does not seem to contribute significantly to the observed increase in IK. In addition, although Goto et al (1983), Umeno (1984) and Brown & DiFrancesco (1980) have suggested previously that the ISO-induced increase in Ic. may be essential for the augmentation of IK' our results did not confirm this.…”

The transduction system in the isoproterenol activation of the Ca(2+)-activated K+ channel in guinea pig taenia coli myocytes.

“…[3-Adrenergic agonists increase the potassium current (IK) of cardiac myocytes (e.g., Brown and Noble, 1974;Umeno, 1984;Bennett and Begenisich, 1987;Walsh and Kass, 1988), possibly through a process involving cAMP-dependent phosphorylation (by protein kinase A) of the relevant protein (Tsien, Giles, and Greengard, 1972; Brum, Flockerzi, Hofmann, Osterrieder, and Trautwein, 1983;Kameyama, Hescheler, Hofmann, and Trautwein, 1986;Walsh and Kass, 1988). However, there are indications that IK may also be regulated by protein kinase C as well as by protein kinase A (Tohse, Kameyama, and Irisawa, 1987;Walsh and Kass, 1988).…”