Session Speaker

Does the Renin - Angiotensin System (RAS) Regulate Also Intraocular Pressure (IOP)
Heikki Ilmari Vapaatalo, Anu Vaajanen, Päivi Alajuuma and Olli Oksala
Finland

The central role of RAS in the regulation of blood pressure is widely accepted and drugs which inhibit the formation of the potent vasoconstrictor angiotensin II (AngII) i.e. ACE inhibitors or drugs which block the Ang receptors of type1 form the cornerstone in the treatment of hypertension. However, from AngI and AngII also vasodilating and blood pressure lowering products, such as Ang(1-7) are formed by another ACE iso-enzyme (ACE2). Ang(1-7) acts by stimulating newly described, vasodilatory and antiproliferative Mas-receptors. Furthermore, AngII itself has also vasodilatory and antiproliferative receptors (AT2R).

We and others have described different components of RAS in various parts of the eye. It can be suggested that these components act on IOP either by reducing aqueous humour formation or by increasing its outflow or both.
Evidence for this suggestion is as follows:

1. ACE2 enzyme activity was found in retina and in ciliary body more than in vitreous (porcine). 2. Mas receptors were present in different parts of the eye, in retina more than in ciliary body (rat). The level of Mas receptors was approximately half of the AT1R:s and twice that of AT2R:s.
3. Ang(1-7) reduced IOP in normotensive eyes without influence on aqueous humour outflow facility (rabbit).
4. A relationship between the development of systemic hypertension and increased IOP was found (spontaneously hypertensive rats, SHR).

In conclusion, molecules which increase the intraocular ACE2 activity and thus formation of Ang(1-7) or activate Mas receptors are a facinating option for development of new antiglaucoma drugs.

Grants: Päivikki and Sakari Sohlberg Foundation, The Eye Foundation, The Glaucoma Research Foundation, Finland