title: Neurogenic contractions in intraocular porcine ciliary arteries are mediated by α₂-adrenoceptors and NPY₁ receptors and are inhibited by prostaglandin E₂ acting on prejunctional EP₄ receptors.
abstract: Prostaglandin analogues and adrenergic drugs are used to reduce the intraocular pressure in glaucoma, which may partly be due to an effect on the tone of the intraocular arteries supplying the ciliary body. The aim of the present study was to investigate the interaction between prostaglandins and autonomic nervous activity induced by electrical stimulation of the tone in these ciliary vessels. The intraocular part of porcine ciliary arteries were isolated and mounted in a microvascular myograph for isometric tension recordings, and the effect of prostaglandin E(2) on electrically induced contractions was studied in the presence of selective EP receptor antagonists. PGE(2) induced concentration-dependent inhibition of electrically induced contractions of intraocular ciliary arteries which depended on the presence of the vascular endothelium. The effect of PGE(2) was blocked by an EP(4) receptor antagonist but not by an EP(1) receptor antagonist. The neurogenic contractions were partially inhibited by an α(2)-adrenoceptor antagonist and totally inhibited by a NPY(1) receptor antagonist. The effect of these antagonists was similar when contraction was induced by noradrenaline and NPY. Neurogenic contractions in intraocular porcine arteries are mediated by α(2)-adrenoceptors and NPY(1) receptors and can be inhibited by PGE(2) acting on prejunctional EP(4) receptors. This contributes to a further understanding of the role of the autonomic nervous system and prostaglandins for regulating blood flow to the anterior segment of the eye.
authors.affiliation: Department of Ophthalmology, Aarhus University Hospital, Norrebrogade 44, 8000 Aarhus C, Denmark. sidse@kringelholt.dk
authors.forename: Sidse
authors.initials: S
authors.lastname: Kringelholt
authors.forename: Ulf
authors.initials: U
authors.lastname: Simonsen
authors.forename: Toke
authors.initials: T
authors.lastname: Bek
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D019842:Ciliary Arteries / Q000502:physiology*; D015232:Dinoprostone / Q000494:pharmacology*; D004558:Electric Stimulation; D004730:Endothelium, Vascular / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000378:metabolism; D019335:Nitroarginine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism*; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors / Q000378:metabolism*; D058309:Receptors, Prostaglandin E, EP4 Subtype / Q000378:metabolism*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013552:Swine; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000319:Adrenergic beta-Antagonists; D004791:Enzyme Inhibitors; D018341:Receptors, Adrenergic, alpha-2; D017476:Receptors, Neuropeptide Y; D058309:Receptors, Prostaglandin E, EP4 Subtype; D026941:Sodium Channel Blockers; C097212:neuropeptide Y-Y1 receptor; D019335:Nitroarginine; D013779:Tetrodotoxin; D011433:Propranolol; D015232:Dinoprostone; D009638:Norepinephrine