Pharmacological and electrophysiological discrimination of contractile responses to selective .ALPHA.1- and .ALPHA.2-adrenoceptor agonists in rat tail artery.
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Pharmacological and electrophysiological properties of postsynaptic α-adrenoceptor subtypes in rat tail artery were compared using selective α<SUB>1</SUB> and α<SUB>2</SUB>-adrenoceptor agonists. Five α-adrenoceptor agonists contracted the tail artery with the following order of maximal effects: norepinephrine (α<SUB>1</SUB> and α<SUB>2</SUB>)>methoxamine (α<SUB>1</SUB>)=phenylephrine (α<SUB>1</SUB>)>>clonidine (α<SUB>2</SUB>)>UK-14, 304 (α<SUB>2</SUB>). Phenoxybenzamine greatly diminished contractions induced by methoxamine and phenylephrine, but had little effect on responses to UK-14, 304. Idazoxan antagonized more potently against UK-14, 304 than against methoxamine. These results suggest the heterogeneity of postsynaptic α-adrenoceptors in the rat tail artery. Furthermore, responses to methoxamine and phenylephrine 1) had faster onsets and 2) were more resistant to Ca<SUP>2+</SUP> entry blockers, nicardipine and diltiazem, and a promotor, Bay K 8644, or decreasing of extracellular Ca<SUP>2+</SUP> and 3) were more sensitive to a calmodulin antagonist, W-7, than the responses to UK-14, 304 and clonidine. Both methoxamine and UK-14, 304 depolarized the membrane but methoxamine produced stronger depolarization than UK-14, 304. Therefore, the high sensitivity of α<SUB>2</SUB>-adrenoceptor agonists-induced responses to Ca<SUP>2+</SUP> entry blockers and promotors cannot be accounted for solely by membrane depolarization. These results may indicate the differences in the Ca<SUP>2+</SUP> movement for the contractions produced by α<SUB>1</SUB>- and α<SUB>2</SUB>-adrenoceptor agonists.
- 公益社団法人 日本薬理学会の論文
公益社団法人 日本薬理学会 | 論文
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