The effects of the nitrovasodilator, sodium azide, on intraocular pressure
(IOP) and ciliary vascular tone were compared. IOP was measured in the bovi
ne isolated eye that was perfused via the ciliary artery. Separately, vasod
ilator effects were assessed after raising the vascular tone using noradren
aline (10 muM). Aqueous humor formation (AHF) rate was estimated by a fluor
escein dilution method. Cyclic GMP in the ciliary processes was measured by
radioimmunoassay.
When compared with controls, sodium azide (10 nmole bolus dose) was found t
o lower IOP (2.2 +/- 0.3 mm Hg; P < 0.01) via a reduction in AHF (12.19 +/-
0.26 mul/min to 6.36 +/- 0.53 mul/min; P < 0.001). Azide (1 mu mole) also
reduced ciliary vascular resistance (81.0 +/- 5.5%; P < 0.01). However, the
drug was 20x more potent as an ocular hypotensive than as a vasodilator (E
D50 0.28 nmole on IOP, 5.55 nmole on vascular effect). Azide (10 nmole) als
o increased levels of ciliary cyclic GMP (127 +/- 17 fmol/mg protein to 233
+/- 27 fmol/mg protein, P < 0.01).
The IOP-lowering effect of azide does not appear to depend on its ability t
o activate guanylyl cyclase (GC) in vascular smooth muscle, but rather is l
ikely a consequence of direct activation of ciliary epithelial GC.