**10. Carbonic anhydrase inhibitors**

The hypotensive effect of carbonic anhydrase inhibitors is a result of reduction of aqueous humour production at the ciliary epithelium level. However in cultured retinal cells, RGC death is prevented by dorzolamide because of its anti-apoptotic pathway [60].


**Table 1.** Pharmacological neuroprotection strategies

blocks the voltage gated calcium current. High intracellular calcium can be neurotoxic. Due to the Ca2+ channel blockage activity by the selective beta 1 beta blocker, betaxolol exerts a neuroprotective effect on the retinal ganglion cells. This effect can be seen at 2-50uM concen‐ tration [53]. Timolol is not effective even in higher concentrations (100uM) and clinically betaxolol is more efficacious in preserving visual fields in glaucoma patients compared to timolol [54]. It has been demonstrated in human cryopreserved retinal arterioles that intralu‐ minal bextaolol caused a significant greater dilatation than timolol, this may be due to the

Betaxolol 0.5% also upregulates the neurotrophic factor BDNF in retinal glia cells [56]. By its action on vascular smooth muscle relaxation this improves blood flow and reduces ischemia induced RGC apoptosis [52, 57]. Retinal ganglion cells protection has been shown using rat experimental model and the preservation of the a and b waves in the electroretinogram in both ischemic-reperfusion and glutamate toxicity models [56,57,58]. This has also been seen in light

As high intracellular calcium can be neurotoxic reducing this effect can be neuroprotective to

Prostaglandin analogs are known as a first line treatment for reducing the IOP. Howev‐ er, latanoprost and bimatoprost acid have shown a neuroprotective on hypoxic induced or glutamate exocitoxity on RGCs [58,59]. This was IOP independent and is not thought to be associated with normal mechanism to lower IOP [59]. Acting via prostaglandin F2 receptors, it has been suggested that latanoprost may have a COX 2 feedback inhibition resulting in neuroprotection [58]. It has also been shown that it inhibits inducible NOS [56]. Latanoprost may also be combined with the NO moiety as previously mentioned [38,39]. Further, it has been theorized that it may have an anti apoptotic effect through the

The hypotensive effect of carbonic anhydrase inhibitors is a result of reduction of aqueous humour production at the ciliary epithelium level. However in cultured retinal cells, RGC

death is prevented by dorzolamide because of its anti-apoptotic pathway [60].

the cells. This effect can be seen in both beta blockers and alpha agonists [2] (Table 1).

response experiments on tiger salamander flat mounted retinas [53].

selective nature of the beta blocker [55]

210 Glaucoma - Basic and Clinical Aspects

**8. Calcium channel blockade**

**9. Prostaglandin analogs**

inhibition of caspase-3 [58,60].

**10. Carbonic anhydrase inhibitors**
