ATC Group: S01E Antiglaucoma preparations and miotics
Anatomical Therapeutic Chemical Classification System
Aceclidine acts as a muscarinic acetylcholine receptor agonist and is a parasympathomimetic miotic agent used in the treatment of narrow angle glaucoma. It decreases intraocular pressure.
Acetazolamide is an enzyme inhibitor which acts specifically on carbonic anhydrase. By inhibiting the reaction catalysed by this enzyme in the renal tubules, acetazolamide increases the excretion of bicarbonate and of cations, chiefly sodium and potassium, and so promotes alkaline diuresis. By inhibiting carbonic anhydrase in the eye acetazolamide decreases intra-ocular pressure and is therefore useful in the treatment of glaucoma.
Acetylcholine is a physiological neuromediator of postganglionic parasympathetic nerve fibres (muscarinic action), skeletal muscles and ganglia of the sympathetic system (nicotinic action).
Apraclonidine is an α2-adrenergic receptor agonist and a weak α1-adrenergic receptor agonist. It is used for the prevention and treatment of postsurgical intraocular pressure elevation.
Betaxolol is a cardioselective Beta1 receptor blocker which, when applied topically to the eye, lowers intraocular pressure. It is thought to produce this effect by reducing the rate of production of aqueous humour.
Bimatoprost is a potent ocular hypotensive agent. It is a synthetic prostamide, structurally related to prostaglandin F2α (PGF2α), that does not act through any known prostaglandin receptors.
Brimonidine is an alpha2-adrenergic receptor agonist that is 1000-fold more selective for the alpha2-adrenoceptor than the alpha1-adrenoreceptor. This selectivity results in no mydriasis and the absence of vasoconstriction in microvessels associated with human retinal xenografts.
Brinzolamide is an inhibitor of carbonic anhydrase II (CA-II). Carbonic anhydrase (CA) is an enzyme found in many tissues of the body, including the eye. Inhibition of carbonic anhydrase in the ciliary processes of the eye decreases aqueous humour secretion resulting in a reduction in intraocular pressure (IOP) which is a major risk factor in the pathogenesis of optic nerve damage and glaucomatous visual field loss.
Carbachol is a potent cholinergic (parasympathomimetic) agent which produces constriction of the iris and ciliary body resulting in reduction in intraocular pressure (IOP).
Carteolol is a non-selective beta-adrenergic blocking agent with associated intrinsic sympathomimetic activity (ISA) and without significant membrane stabilizing activity. Carteolol reduces normal and elevated intraocular pressure whether or not accompanied by glaucoma.
Clonidine has been shown to have both central and peripheral sites of action. With long-term treatment clonidine reduces the responsiveness of peripheral vessels to vasoconstrictor and vasodilator substances and to sympathetic nerve stimulation. Early in treatment, however, blood pressure reduction is associated with a central reduction of sympathetic outflow and increased vagal tone.
Dichlorphenamide is a carbonic anhydrase inhibitor. However, the precise mechanism by which dichlorphenamide exerts its therapeutic effects in patients with periodic paralysis is unknown.
Dorzolamide is a potent inhibitor of human carbonic anhydrase II. Following topical ocular administration, dorzolamide reduces elevated intra-ocular pressure, whether or not associated with glaucoma.
Epinephrine is a direct acting sympathomimetic agent, which exerts effects on both α and β adrenoceptors. It has more pronounced effects on β than on α adrenoceptors, although α effects prevail at high doses. The effects of adrenaline include increased rate and force of cardiac contraction, cutaneous vasoconstriction and broncho-dilatation.
Guanethidine is a antihypertensive drug. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues. It is taken up by norepinephrine transporters. It becomes concentrated in norepinephrine transmitter vesicles, replacing norepinephrine in these vesicles.
The active substance latanoprost, a prostaglandin F2α analogue, is a selective prostanoid FP receptor agonist which reduces the IOP by increasing the outflow of aqueous humour.
Latanoprostene bunod is thought to lower intraocular pressure by increasing outflow of aqueous humor through both the trabecular meshwork and uveoscleral routes. Intraocular pressure is a major modifiable risk factor for glaucoma progression. Reduction of intraocular pressure reduces risk of glaucomatous visual field loss.
Levobunolol is a non-cardioselective beta-adrenoceptor blocking agent, equipotent at both beta1 and beta2 receptors. The primary mechanism of action of levobunolol in reducing intraocular pressure is most likely a decrease in aqueous humor production. Levobunolol reduces intraocular pressure with little or no effect on pupil size in contrast to the miosis which cholinergic agents are known to produce.
Neostigmine inhibits cholinesterase activity and prolongs and intensifies the muscarinic and nicotinic effects of acetylcholine. The anticholinesterase actions of neostigmine are reversible.
Netarsudil is a rho kinase inhibitor, which is believed to reduce intraocular pressure (IOP) by increasing the outflow of aqueous humor through the trabecular meshwork. The exact mechanism is unknown.
Physostigmine is a reversible inhibitor of acetylcholinesterase. As an inhibitor of acetyl-cholinesterase, physostigmine slows down the degradation of acetylcholine and acts like an indirect parasympathomimetic drug due to an increase of the acetylcholine concentration at the receptor.
Pilocarpine is a cholinergic parasympathomimetic agent exerting a broad spectrum of pharmacologic effects with predominant muscarinic action. Pilocarpine, in appropriate dosage, can increase secretion by exocrine glands such as the sweat, salivary, lacrimal, gastric, pancreatic and intestinal glands and the mucous cells of the respiratory tract.
Tafluprost is a fluorinated analogue of prostaglandin F2α. Tafluprost acid, the biologically active metabolite of tafluprost, is a highly potent and selective agonist of the human prostanoid FP receptor.
Timolol is a non-selective beta-adrenergic receptor blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anaesthetic activity. Timolol reduces intra-ocular pressure, whether or not this is associated with glaucoma.