Interaction between adenosine and beta-adrenoceptors.

Saito, Daiji; Mima, Tsutommu; Uchida, Shunya; Obayashi, Naotsugu; Marutani, Morio; Mukohara, N; Kusachi, Shozo; Tsuji, Takao; Haraoka, Shoichi

doi:10.1253/jcj.55.81

Cited by 3 publications

(3 citation statements)

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“…6). This conclusion is supported by previous reports that the stimulatory effect of isoproterenol on myocardial contractility is not inhibited by adenosine and A 1 AdoR agonists in vivo (16,23,24) and is maintained in mouse hearts overexpressing A 1 AdoRs (9).…”

Section: Discussionsupporting

confidence: 88%

“…Use of animals in the present study was in accordance with the Guide for the Care and Use of Laboratory Animals (National Institutes of Health Publication No. 86- 23,1985) and was approved by the Institutional Animal Care and Use Committee of the University of Florida. Single ventricular myocytes were isolated from the hearts of adult Harlan guinea pigs of either sex, as described previously (26).…”

Section: Methodsmentioning

confidence: 99%

“…Consistent with the anti-␤-adrenergic actions of adenosine, an inhibition by adenosine of isoproterenol-facilitated ventricular tachycardia has been demonstrated in patients (19). However, when applied at therapeutic or "physiological" concentrations, adenosine did not significantly attenuate isoproterenol-stimulated contractility in vivo, and thus the physiological significance of anti-␤-adrenergic actions of adenosine was questioned (16,23,24). Because these apparently conflicting results were obtained by measurement of different responses (electric activity versus contractility), it is possible that the ␤-adrenoceptor-mediated arrhythmic and inotropic effects of catecholamines are not equally antagonized by adenosine.…”

mentioning

confidence: 93%

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Selective attenuation by adenosine of arrhythmogenic action of isoproterenol on ventricular myocytes

Song¹,

Shryock²,

Knot

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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We examined whether adenosine equally attenuated the stimulatory effects of isoproterenol on arrhythmic activity and twitch shortening of guinea pig isolated ventricular myocytes. Transmembrane voltages and whole cell currents were recorded with patch electrodes, and cell twitch shortening was measured using a video-motion detector. Isoproterenol increased the action potential duration at 50% repolarization (APD50), L-type Ca2+ current [I(Ca(L))], and cell twitch shortening and induced delayed afterdepolarizations (DAD), transient inward current (I(Ti)), and aftercontractions. Adenosine attenuated the arrhythmogenic actions of isoproterenol more than it attenuated the effects of isoproterenol on APD50, I(Ca(L)), or twitch shortening. Adenosine (0.1-100 micromol/l) decreased the amplitude of DADs by 30 +/- 6% to 92 +/- 5% but attenuated isoproterenol-induced prolongation of the APD50 by only 14 +/- 4% to 59 +/- 4% and had no effect on the voltage of action potential plateau. Adenosine (30 micromol/l) inhibited I(Ti) by 91 +/- 4% but decreased isoproterenol-stimulated I(Ca(L)) by only 30 +/- 12%. Isoproterenol-induced aftercontractions were abolished by adenosine (10 micromol/l), whereas the amplitude of twitch shortening was not reduced. The effects of adenosine on twitch shortenings and aftercontractions were mimicked by the A1-adenosine receptor agonist CPA (N6-cyclopentyladenosine) and by ryanodine. In conclusion, adenosine antagonized the proarrhythmic effect of beta-adrenergic stimulation on ventricular myocytes without reducing cell twitch shortening.