Graefe's Archive for Clinical and Experimental Ophthalmology

, Volume 241, Issue 3, pp 226–231

Muscarinic blockers potentiate β-adrenergic relaxation of bovine iris sphincter

Authors

  • Ayelet Barilan
    • Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
  • Rachel Nachman-Rubinstein
    • Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
  • Yoram Oron
    • Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
  • Orna Geyer
    • Department of Ophthalmology, Carmel Medical Center, 7 Michal Street, Haifa, Israel
Laboratory Investigation

DOI: 10.1007/s00417-002-0572-x

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

Abstract

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.

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© Springer-Verlag 2003