Glibenclamide and L-NG-nitro-arginine methyl ester modulate the ocular and hypotensive effects of calcitonin gene-related peptide.

Calcitonin gene-related peptide (CGRP) given i.v. to rabbits induced hypotension and a breakdown of the blood-aqueous barrier. Glibenclamide, a blocker of ATP-sensitive K+ (K+ATP) channels antagonized both these effects. The K+ATP channel opener diazoxide reduced blood pressure but did not damage the blood-aqueous barrier. Inhibition of nitric oxide synthase antagonized the effects of CGRP on the blood-aqueous barrier but did not attenuate the hypotensive response. The results suggest that vasodilatation induced by the opening of K+ATP channels is a prerequisite for the effect of CGRP on the blood-aqueous barrier.