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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Prejunctional alpha 2-adrenoceptor mediated inhibitory action of clonidine and B-HT 920, but not urapidil in guinea pig ileum.

Isolated guinea pig ileal longitudinal muscle was stimulated transmurally with a frequency of 0.1 Hz, duration of 0.5 msec, and supramaximal voltage (80-100 V). Transmural stimulation induces ileal contractions via activation of cholinergic neurons. alpha 2-Adrenergic agonists block the response to transmural stimulation via activation of prejunctional alpha 2 receptors which inhibit release of acetylcholine from cholinergic nerve terminals. Urapidil has been reported to have alpha 2-agonistic actions, and therefore was compared to the prototypic alpha 2 agonists, clonidine and B-HT 920. Clonidine and B-HT 920 depressed responses to transmural stimulation in the guinea pig ileum. Clonidine was the most potent inhibitor of the contractions, followed closely by B-HT 920. Very high concentrations of urapidil were necessary to suppress nerve-induced contractions of the ileum. The effects of clonidine and B-HT 920, but not urapidil, were antagonized by the selective alpha 2 antagonist, yohimbine. In unstimulated preparations, in which exogenous acetylcholine was used to elicit contractions of the ileum, urapidil depressed the response while clonidine and B-HT 920 had no effect. When PGF1 alpha was used to contract the ileum, no inhibitory effects were noted for urapidil, clonidine, or B-HT 920. Therefore urapidil, only in high concentrations, inhibits the contraction to transmural stimulation by depressing the response at a postjunctional cholinergic site. No evidence was found that urapidil can act as an agonist at a prejunctional alpha 2-receptor site.[1]

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