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.
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology*; D003981:Diazoxide / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology*; D007022:Hypotension / Q000139:chemically induced; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase; D015221:Potassium Channels / Q000187:drug effects; D011817:Rabbits; D014602:Uvea / Q000098:blood supply* / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D015221:Potassium Channels; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D015740:Calcitonin Gene-Related Peptide; D003981:Diazoxide; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester