Abstract
Purpose :
Ripasudil (K-115) is a Rho-kinase inhibitor and is an ocular hypotensive agent. Ripasudil also has a vasodilating effect. The optic disc blood flow is supplied by posterior ciliary arteries (PCAs). This study aimed to clarify the vasodilatory effect of exogenous Ripasudil on isolated PCAs.
Methods :
Vascular ring segments were mounted on a double myograph system. After obtaining the maximal contraction following the administration of a high-K solution, different concentrations of Ripasudil (100 nM to 100 μM) were administrated. When a vasodilatory effect was observed, carboxy-2-phenyl-4,4,5,5,-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO), a nitric oxide scavenger, or NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, were administered. All isometric force measurements are given as relative values compared with high-K–induced maximal contractions.
Results :
Ripasudil significantly relaxed high-K solution-induced contracted rabbit PCAs in a concentration dependent manner (100 nM [34.8%±3.5]; 1 μM [78.5±17.3]; 10 μM [91.68±9.0]; 100 μM [94.41±8.3]). Carboxy-PTIO (1 mM) or L-NAME (300 mM) did not inhibit Ripasudil-induced relaxation in rabbit PCAs.
Conclusions :
Ripasudil has a nitric oxide independent vasodilatory effect on high K-induced contractions in isolated rabbit PCAs.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.