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Publication : ATP-sensitive potassium (K(ATP)) channel openers diazoxide and nicorandil lower intraocular pressure in vivo.

First Author  Chowdhury UR Year  2013
Journal  Invest Ophthalmol Vis Sci Volume  54
Issue  7 Pages  4892-9
PubMed ID  23778875 Mgi Jnum  J:214190
Mgi Id  MGI:5588542 Doi  10.1167/iovs.13-11872
Citation  Chowdhury UR, et al. (2013) ATP-sensitive potassium (K(ATP)) channel openers diazoxide and nicorandil lower intraocular pressure in vivo. Invest Ophthalmol Vis Sci 54(7):4892-9
abstractText  PURPOSE: To evaluate the expression of ATP-sensitive potassium (K(ATP)) channel subunits and study the effect of K(ATP) channel openers diazoxide and nicorandil on intraocular pressure (IOP) in an in vivo mouse model. METHODS: Expression of K(ATP) channel subunits in normal C57BL/6 mouse eyes was studied by immunohistochemistry and confocal microscopy. Wild-type C57BL/6 mice were treated with K(ATP) channel openers diazoxide (n = 10) and nicorandil (n = 10) for 14 days. Similar treatments with diazoxide were performed on K(ir)6.2((-/-)) mice (n = 10). IOP was recorded with a handheld tonometer 1 hour, 4 hours, and 23 hours following daily treatment. Posttreatment histology was examined by light and transmission electron microscopy. RESULTS: The K(ATP) channel subunits SUR2B, K(ir)6.1, and K(ir)6.2 were identified in all tissues within mouse eyes. Treatment with diazoxide in wild-type mice decreased IOP by 21.5 +/- 3.2% with an absolute IOP reduction of 3.9 +/- 0.6 mm Hg (P = 0.002). Nicorandil also decreased IOP (18.9 +/- 1.8%) with an absolute IOP reduction of 3.4 +/- 0.4 mm Hg (P = 0.002). Treatment with diazoxide in K(ir)6.2((-/-)) mice had no effect on IOP. No morphological abnormalities were observed in diazoxide- or nicorandil-treated eyes. CONCLUSIONS: K(ATP) channel openers diazoxide and nicorandil are effective regulators of IOP in mouse eyes. K(ir)6.2 appears to be a major K(ATP) channel subunit through which IOP is lowered following treatment with diazoxide.
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