Abstract
Adenylate cyclase activity in rabbit retinal homogenates can be stimulated directly by forskolin or through a receptor-mediated mechanism by vasoactive intestinal peptide (VIP). In contrast the α 2-adrenoceptor agonists clonidine and UK-14,304 reduce the basal cAMP level slightly. This was more evident following application of forskolin and VIP where the decrease of cAMP caused by clonidine and UK-14,304 is dose-dependent. The α 2-adrenoceptor agonist response is blocked by pertussis toxin and is insensitive to the phosphodiesterase inhibitor, isobutylmethylxanthine, suggesting the involvement of a G i-protein. Clonidine and UK-14,304 attenuation of elevated cAMP levels can be inhibited by the α 2-receptor antagonist yohimbine and phentolamine but not by the specific α 1-receptor antagonist, prazosin. Serotonergic, cholinergic and β-adrenergic receptor antagonists were without effect. The results demonstrate that α 2-adrenergic receptors in the retina exert inhibitory effects on adenylate cyclase activity mediated by an inhibitory guanine nucleotide regulating protein.
Published Version
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