Glaucoma is an optic neuropathy characterised by optic nerve degeneration associated with
visual field defects. It remains the world’s number one cause of irreversible blindness and
patients usually present at late stage of the disease since it is generally asymptomatic until
severe. The disease is subdivided into primary and secondary with primary open-angle
glaucoma (POAG) being the most common type. At present, lowering the intraocular pressure
(IOP) remains the only proven efficient approach in delaying the onset or preventing the
progression of the disease. Medical treatment with topical antiglaucoma agents is the
treatment of choice in open angle glaucoma. The use of antiglaucoma drugs aims to reduce
IOP by enhancing aqueous humour (AH) outflow, reducing AH production, or both. The choice
to use any available treatment option should be carefully considered in an attempt to maximise
benefits and reducing the risk of developing adverse drug reactions. This review highlights the
six classes of ocular hypotensive agents currently in use for POAG treatment including
prostaglandin analogues; -adrenergic receptor blockers; -2 adrenergic receptor stimulants;
carbonic anhydrase inhibitors; muscarinic receptor stimulants; rho kinase inhibitors with
regards to their mechanism/s of action and potential adverse drug reactions, and
antiglaucoma fixed drug combinations.
1 Interaction between renin-angiotensin (RAS) and sympathetic nervous systems (SNS) was investigated by examining the effect of cumulative blockade of angiotensin II (Ang II) and adrenergic receptors in normal Sprague Dawley rats. 2 Rats were treated with losartan (10 mg/kg), carvedilol (5 mg/kg), or losartan plus carvedilol (10+5 mg/kg) orally for 7 days. On day 8, the animals were anaesthetized with pentobarbitone and prepared for systemic haemodynamic study. Dose-response relationships for the elevation of mean arterial pressure or change in heart rate (HR) in response to intravenous injections of noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined. 3 Losartan or the combination of losartan with carvedilol blunted vasopressor responses to ME and Ang II. Dose-response relationships for agonist action on HR were significantly inhibited by all treatments except for the combination of losartan and carvedilol on the decrease in HR induced by PE. Carvedilol decreased vasopressor responses to NA, PE and Ang II, and HR responses to NA, ME and Ang II. Combination treatment produced similar effects to losartan on the vasopressor and HR responses but had a greater effect on vasopressor responses to ME and Ang II, and on HR responses to NA and Ang II than carvedilol alone. 4 It is concluded that peripheral vasoconstriction induced by Ang II is partly mediated by adrenergic action and that the vasopressor responses to adrenergic agonists depend on an intact RAS. These observations suggest an interactive relationship between RAS and SNS in determining systemic haemodynamic responses in 'normal' rats.