Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Groschner, K; Kukovetz, WR.
Carbachol inhibits atrial contractility in the presence of potassium channel blocking agents.
J Cardiovasc Pharmacol. 1989; 14(4):648-652
Doi: 10.1097/00005344-198910000-00018
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- Führende Autor*innen der Med Uni Graz
- Groschner Klaus
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- Abstract:
- To elucidate the role of potassium channel activation in muscarinic inhibition of atrial contractility, we studied the influence of K+ channel blockers on the effects of the muscarinic agonist carbachol in isolated guinea pig auricles. We tested BaCl2, tetraethylammoniumchloride (TEA), and 9-aminotetrahydroacridine (THA), which block K+ channels, for their ability to antagonize the effects of carbachol on atrial contractility and functional refractory period. Due to inhibition of K+ outward currents, BaCl2, TEA, and THA markedly blocked the carbachol-induced shortening of refractory period and, to a lesser extent, antagonized its negative inotropic action. BaCl2, TEA, and THA shifted the concentration-response curve of the negative inotropic action of carbachol to the right; the most pronounced effect was obtained with TEA (DR = 30 at 3 x 10(-3) M). The maximum negative inotropic effect of carbachol, however, was only slightly reduced by the K+ channel blockers, and carbachol clearly inhibited atrial contractility even in the absence of any shortening of refractory period. These results suggest the existence of an additional cholinergic, negative inotropic mechanism, distinctly different from activation of atrial K+ channels.
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