So then both timolol and epinephrine would block aqueous humor production but epinephrine would be doing it throught its alpha1 mediated effect (vasoconstriction) on the blood vessels supplying the ciliary body whereas timolol would block the beta1 receptors on the cells of the ciliary body.
For epinephrine to have an effect on the alpha1 receptors, we would have to administer a high dose epi, wouldn't we? We also know that even though a high dose epi has a predominantly alpha1 effect, it does also act on beta1 receptors and we do have beta1 receptors in the ciliary body. What puzzles me is if we administer a high dose epi, wouldn't it cause the ciliary body to secrete more aqueous humor while at the same time vasoconstricting the blood vessels supplying it? Or is it that once we have constricted the blood vessels, the cells will not be able to secrete any aqueous humor even though the same epinephrine may be acting on the beta1 receptors on the ciliary body cells and trying to stimulate its release?
Why can we not use epi for narrow angle glaucoma? Is it because it would stimulate the alpha1 receptors on the radial muscles and cause it to contract which would in turn further block the already narrow irido-corneal angle? But using a muscarinic agonist is ok in a case of narrow angle glaucoma because it would contract the ciliary body (and the sphincter muscles) and somehow help in freeing up more space in the irido-corneal angle for the aqueous humor to flow into the trabecular meshwork and then to the canal of schlem?