Sustained decreases in systemic blood pressure do not cause ocular hypotension.

The unilateral, topical administration of certain ocular hypotensive agents, notably clonidine, is reported to result in a bilateral decrease in intraocular pressure. It has been previously proposed that such bilateral ocular hypotensive responses may be centrally mediated. However, the possible influence of blood pressure changes on intraocular pressure has remained a complicating factor in determining mechanisms of action. In order to further clarify the potential relationship between systemic blood pressure changes and intraocular pressure, the effects of two systemic antihypertensive drugs were determined in the conscious rabbit. Topical, unilateral administration of either hydralazine or prizidilol did not lower the intraocular pressure of either eye. A bolus intravenous injection of either hydralazine or prizidilol caused substantial systemic hypotension that persisted for at least 3 h, but no decreases in intraocular pressure occurred. These studies indicate that sustained decreases in systemic blood pressure of approximately 15 mm Hg do not result in ocular hypotension.

Topical timolol, at conventional, unilateral doses causes bilateral ocular beta-blockade in rabbits.

The studies described herein reveal that unilateral 0.3% and 1% doses of timolol produce marked beta-adrenoceptor blockade in treated and in contralateral eyes which did not receive timolol. This indicates that unilateral, conventional topical doses of timolol administered to rabbits cause bilateral ocular beta-adrenoceptor blockade. In addition, 0.1% and 1% doses of timolol applied to one eye resulted in blockade of cardiovascular beta-adrenoceptors. Thus, the most likely explanation for bilateral ocular beta-blockade would be systemic absorption of timolol from the treated eye and redistribution to the fellow eye. Since contralateral eyes would not provide an adequate control in circumstances where a large dose of timolol is administered unilaterally, caution must be exercised in interpreting data obtained in laboratory animals with doses of timolol similar to those employed clinically. A 0.01% dose of timolol appears adequate to achieve marked, unilateral ocular beta-adrenoceptor blockade in rabbits.