In the rat eye, intracameral injections of substance P in doses of 10-30 pmol caused a maximal long-lasting miosis and a leakage of plasma proteins into the aqueous humor, indicating a breakdown of the blood-aqueous barrier. Neurokinin A seemed equipotent to SP, but calcitonin-gene-related peptide (CGRP) (17 pmol) caused neither miosis nor protein leakage into the aqueous humor. The same result was obtained when CGRP was administered intravenously. Intracameral injection of capsaicin caused only a transient miosis which could not be repeated with further injections, even though the pupillary sphincter was still able to react to exogenous SP. Antidromic electrical stimulation of the trigeminal nerve caused plasma extravasation in the skin and a breakdown of the blood-aqueous barrier with an increased protein content in the aqueous humor. The stimulation did not affect the pupil size. The results indicate that in rat eyes SP and NKA are miotics, but the amounts that can be released from sensory nerve endings are too small to cause persistent miosis. These peptides are more likely to play a role in the neurogenic breakdown of the blood-aqueous barrier. CGRP at the same dose affects neither the pupillary sphincter muscle nor the barrier.