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Modulation of iris sphincter and ciliary muscles by Urocortin 2
Author(s) -
Rocha De Sousa A.,
Ferreira D.,
TavaresSilva M.,
Raimundo A.R.,
BarbosaBreda J.,
LeiteMoreira A.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.0f085
Subject(s) - urocortin , carbachol , contraction (grammar) , medicine , endocrinology , sphincter , contractility , chemistry , nitric oxide , ciliary muscle , muscle contraction , isometric exercise , muscle relaxation , biology , anatomy , stimulation , neuroscience , receptor , accommodation
Purpose Urocortin 2 ( UCN 2) is a peptide related to corticotropin‐releasing factor, capable of activating CRF ‐R2. Among its multisystemic effects, it has actions in all 3 muscle subtypes, either increasing or decreasing contractility. This study's aim was to determine its potential role in two of the intrinsic eye muscle kinetics and to study the likely subcellular pathways involved. Methods Strips of iris sphincter (rabbit) and ciliary (bovine) muscles were dissected and mounted in isometric force‐transducer systems filled with aerated‐solutions, subjected to 0.5 mN and 1.0 mN preloads, respectively. Contraction was elicited using carbachol (10–6M for iris sphincter, 10–5M for ciliary muscle), prior to all testing substances. Results UCN 2 induced relaxation in iris sphincter muscle, being the effect maximal at 10‐7M concentrations (‐12.2% variation, versus control, n = 6). This effect was abolished with incubation of indomethacin (n = 8), antisauvagine‐30 (n = 7), chelerytrine (n = 6) and SQ 22536 (n = 8), but preserved with L‐nitro‐L‐arginine (n = 9). In carbachol pre‐stimulated ciliary muscle, UCN 2 (10‐5M) enhanced contraction (maximal effect of 18.2% increase, versus control, n = 10 pairs); pre‐contraction studies were negative. Conclusions UCN 2 is a new neurohumoral modulator of iris sphincter relaxation, dependent on CRF ‐R2 activation, synthesis of prostaglandins ( COX pathway) and both adenylate cyclase and PKC signaling pathways, but independent of nitric oxide production. Regarding ciliary muscle, UCN 2 enhances carbachol‐induced contraction, in higher doses.