Does adrenaline modulate the Na+-Ca2+ exchanger in isolated toad pacemaker cells?
beta-Adrenergic stimulation of pacemaker cells from the sinus venosus of the cane toad (Bufo marinus) increases intracellular calcium ([Ca2+]i) and firing rate. The increase in [Ca2+]i could contribute to the increased firing rate by increasing the inward Na+-Ca2+ exchange current (INa-Ca) during diastole. In this study we measured [Ca2+]i and membrane currents in single, isolated, voltage-clamped pacemaker cells. We show that INa-Ca increases during beta-adrenergic stimulation. To test whether this increase in INa-Ca is caused by elevated [Ca2+]i or by changes in the properties of the Na+-Ca2+ exchanger, we made rapid applications of caffeine and plotted the INa-Ca against [Ca2+]i. This relationship was linear during the declining phase of the [Ca2+]i signal caused by caffeine and was not significantly different in the presence or absence of beta stimulation. These results show that INa-Ca is increased during beta-adrenergic stimulation and will contribute to the increased firing rate. However the increase in INa-Ca appears to be a consequence of the increase in [Ca2+]i and is not caused by changes in the intrinsic properties of the Na+-Ca2+ exchanger.
Department of Physiology, University of Sydney (F13), Sydney, NSW 2006, Australia.
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D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002024:Bufo marinus; D002118:Calcium / Q000378:metabolism; D004553:Electric Conductivity; D004837:Epinephrine / Q000494:pharmacology*; D006321:Heart / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D007700:Kinetics; D009206:Myocardium / Q000166:cytology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D019831:Sodium-Calcium Exchanger / Q000187:drug effects* / Q000502:physiology*
D000318:Adrenergic beta-Agonists; D011943:Receptors, Adrenergic, beta; D019831:Sodium-Calcium Exchanger; D007545:Isoproterenol; D002118:Calcium; D004837:Epinephrine