Overview

Production rate≈2–3 µL/min

Total volume≈0.3 mL (AC ≈0.25 mL, PC ≈0.06 mL)

Turnover time≈100 min

Normal IOP10–21 mmHg (mean ≈15–16)

Trabecular : uveoscleral outflow≈80–90% : 10–20%

Production. Aqueous is formed by the non-pigmented ciliary epithelium through three mechanisms: active secretion (the major part, ≈70–80% — Na⁺/K⁺-ATPase, Cl⁻ and bicarbonate transport with carbonic anhydrase, water following osmotically via aquaporins), ultrafiltration from the fenestrated capillaries of the ciliary processes, and diffusion. Production is ≈2–3 µL/min, higher in the morning and falling by about half during sleep; the ≈0.3 mL total volume turns over roughly every 100 minutes.

Composition. Compared with plasma it has very little protein (≈1% of plasma level, maintained by the blood–aqueous barrier), but high ascorbate (≈15–20× plasma — an antioxidant and UV filter), and elevated lactate; glucose is slightly lower. It is slightly hypertonic.

Circulation and drainage. Ciliary processes → posterior chamber → through the pupil → anterior chamber → iridocorneal angle → either the conventional (trabecular) pathway — trabecular meshwork → canal of Schlemm → collector channels → aqueous and episcleral veins (≈80–90%, pressure-dependent) — or the uveoscleral (unconventional) pathway — through the ciliary muscle interstitium into the suprachoroidal space and out through the sclera (≈10–20%, largely pressure-independent, higher in the young). The balance of inflow and outflow resistance sets the intraocular pressure (IOP), normally 10–21 mmHg.

Location: Anterior and posterior chambers of the eye (anterior segment).

Function

Nourish and remove waste from the avascular cornea, lens and trabecular meshwork
Maintain intraocular pressure and therefore the shape and optics of the globe
Provide a transparent, refractive medium (refractive index ≈1.336)
Antioxidant protection (ascorbate) and immune defence

Physiology: Goldmann equation: IOP = (F − U)/C + Pv, where F = aqueous formation, U = uveoscleral outflow, C = trabecular outflow facility and Pv = episcleral venous pressure (≈8–10 mmHg). IOP shows a diurnal variation of ≈3–5 mmHg, often highest in the early morning.
Secretions: Produced by the non-pigmented ciliary epithelium at ≈2–3 µL/min.
Regulation: Production is increased by β-adrenergic stimulation and reduced by β-blockers, α₂-agonists and carbonic anhydrase inhibitors; it falls during sleep. Outflow increases with ciliary muscle contraction (cholinergic agonists) and with prostaglandin F₂α analogues (uveoscleral route).

Clinical significance

Glaucoma drugs and their targets

Reduce production: β-blockers (timolol — caution in asthma/heart block), carbonic anhydrase inhibitors (dorzolamide topically, acetazolamide orally), α₂-agonists (brimonidine, also increases uveoscleral outflow). Increase outflow: prostaglandin analogues (latanoprost — first line; side-effects: iris darkening, eyelash growth), muscarinic agonists (pilocarpine), Rho-kinase inhibitors (netarsudil). Osmotic agents (mannitol) draw water from the vitreous in acute attacks.

Tonometry

IOP is measured by Goldmann applanation tonometry (gold standard), rebound or air-puff tonometry. A thin cornea causes underestimation of true IOP. Ocular hypertension (IOP >21 mmHg without optic nerve damage) is a risk factor for, but not the same as, glaucoma; normal-tension glaucoma occurs with IOP in the normal range.

Test yourself

Through which route does most aqueous humour leave the eye?

Uveoscleral outflow through the ciliary muscle
Posterior diffusion through the vitreous to the retinal veins
Across the corneal endothelium into the tear film
Trabecular meshwork → canal of Schlemm → episcleral veins

Answer: Trabecular meshwork → canal of Schlemm → episcleral veins

About 80–90% of aqueous drains by the conventional (trabecular) pathway into Schlemm canal and then to aqueous and episcleral veins; ≈10–20% leaves by the uveoscleral route, which prostaglandin analogues enhance.