Secondary neuroprotective effects of hypotensive drugs and potential mechanisms of action

Figures & data

Figure 1. Possible mechanisms of neuroprotection mediated by α₂-adrenergic agonists.

α₂-agonists such as brimonidine initiate multiple possible protective cascades. Direct binding of the α₂-receptor on RGCs could promote Bcl-mediated anti-apoptotic cascades, while binding to receptors expressed by glial or pigment epithelial cells could induce trophic signaling involving BDNF and bFGF, and their respective receptors.

bFGF: Basic FGF; NMDA-R: NMDA receptor; RGC: Retinal ganglion cell.

Figure 2. Putative neuroprotective actions of β-receptor antagonists.

Based on known expression patterns, β-receptor antagonists could bind channels in presynaptic circuits to reduce the release of glutamate and postsynaptic activation of NMDA receptors on RGCs. Antagonists could also exert influence on receptors expressed by vascular elements, leading to increased blood supply and reduced ischemia-related stress. Finally, certain β-receptor antagonists upregulate expression of BDNF in retinal glia.

NMDA-R: NMDA receptor; RGC: Retinal ganglion cell; TRKB: Tyrosine receptor kinase B.

Figure 3. Possible neuroprotective mechanisms of prostaglandin F₂ receptor agonists on retinal ganglion cells.

Evidence suggests a role for prostaglandin agonists in reducing excitotoxic stress. Direct binding of prostaglandin receptors on RGCs could reduce COX-2-mediated induction of nitric oxide synthase.

NMDA-R: NMDA receptor; RGC: Retinal ganglion cell.

Figure 4. Interaction of glutamate with NMDA receptors.

In many neurodegenerative conditions, excessive glutamate release from presynaptic terminals binds to postsynaptic NMDA-Rs, depolarizing the postsynaptic membrane through removal of the Mg²⁺ block. Subsequent influx and build-up of excess calcium leads to excitotoxicity and neuronal apoptosis.

NMDA-R: NMDA receptor.

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