Muscarinic blockers potentiate β-adrenergic relaxation of bovine iris sphincter
- Cite this article as:
- Barilan, A., Nachman-Rubinstein, R., Oron, Y. et al. Graefe's Arch Clin Exp Ophthalmol (2003) 241: 226. doi:10.1007/s00417-002-0572-x
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Background. β-Adrenergic relaxation of iris sphincter has been described in many species, including human. It is generally accepted that the size of the pupil is mainly controlled by muscarinic and α-adrenergic tonus. This study was undertaken to investigate the interactions between muscarinic and β-adrenergic drugs in the relaxation of bovine iris sphincter.
Methods. Intact bovine iris sphincters were incubated in an organ bath and challenged with appropriate β-adrenergic agonists and/or muscarinic antagonists. Tension was measured by a force transducer.
Results. Isolated bovine iris sphincter responded to muscarinic stimulation by contraction and to β-adrenergic stimulation by relaxation. The β-adrenergic agonists isoproterenol (ISO) and salbutamol (SAL) each caused marked relaxation of sphincters pre-contracted with the muscarinic agonist carbamylcholine. Sphincters pre-treated with the muscarinic antagonists atropine (0.1 µM) or ipratropium bromide (10 µM) and challenged 5 min later with either isoproterenol (0.3 nM) or salbutamol (10 nM) exhibited approximately twofold potentiation of β-adrenergic relaxation. Adding the drugs in the reverse order did not produce any potentiation over the effect of β-adrenergic stimulation alone. The dose–response curve to isoproterenol in naive sphincters or sphincters pre-treated with atropine indicated that muscarinic blockade decreased the EC50 rather than potentiated maximal β-adrenergic relaxation.
Conclusion. Muscarinic antagonists potentiate β-adrenergic relaxation of the sphincter by affecting the apparent potency of β-adrenergic agonists and not by antagonizing the intrinsic tonus produced by endogenously released acetylcholine.