The effects of the nitrovasodilator, @entity4627 , on intraocular pressure (IOP) and ciliary vascular tone were compared. IOP was measured in the @entity291 isolated eye that was perfused via the ciliary artery. Separately, vasodilator effects were assessed after raising the vascular tone using @entity1063 (10 microM). @entity7462 formation (AHF) rate was estimated by a @entity941 dilution method. @entity8262 in the ciliary processes was measured by radioimmunoassay. When compared with controls, @entity4627 (10 nmole bolus dose) was found to lower IOP (2.2 +/- 0.3 mm Hg; P < 0.01) via a reduction in AHF (12.19 +/- 0.26 microl/min to 6.36 +/- 0.53 microl/min; P < 0.001). @entity2769 (1 micromole) also reduced ciliary vascular resistance (81.0 +/- 5.5%; P < 0.01). However, the drug was 20x more potent as an ocular @entity551 than as a vasodilator (ED50 0.28 nmole on IOP, 5.55 nmole on vascular effect). @entity2769 (10 nmole) also increased levels of ciliary @entity8262 (127 +/- 17 fmol/mg protein to 233 +/- 27 fmol/mg protein; P < 0.01). The IOP-lowering effect of @entity2769 does not appear to depend on its ability to activate guanylyl cyclase (GC) in vascular smooth muscle, but rather is likely a consequence of direct activation of ciliary epithelial GC.

Intraocular pressure and vascular effects of XXXX in @entity291 perfused eye.

@entity2769 :: ('CHEBI:40910', 'Chemical') :: ['azide', 'Azide'] @entity4627 :: ('MESH:D019810', 'Chemical') :: ['sodium azide'] @entity7462 :: ('MESH:C562390', 'Disease') :: ['Aqueous humor'] @entity551 :: ('MESH:D007022', 'Disease') :: ['hypotensive'] @entity8262 :: ('MESH:D006152', 'Chemical') :: ['Cyclic GMP', 'cyclic GMP'] @entity941 :: ('MESH:D019793', 'Chemical') :: ['fluorescein'] @entity1063 :: ('MESH:D009638', 'Chemical') :: ['noradrenaline'] @entity291 :: ('9913', 'Species') :: ['bovine']
@entity4627 :: (MESH:D019810,Chemical) :: ['sodium azide']
