Expression and function of α1-adrenoceptor subtypes in the porcine renal artery

We investigated the expression and function of α1-adrenoceptor subtypes in the porcine renal artery. Reverse transcription polymerase chain reaction (RT-PCR) and nucleotide sequencing indicated that the mRNAs for α1a- and α1b-adrenoceptors were expressed in the porcine renal artery. Chloroethylclonidine, an α1B- and α1D-adrenoceptor antagonist, partially inhibited the phenylephrine-induced contraction, while 3 nM BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride), an α1D-adrenoceptor antagonist, had no effect. In contrast, 5-methylurapidil, an α1A-adrenoceptor antagonist, induced a rightward shift of the phenylephrine concentration–response curve. The simultaneous measurement of cytosolic Ca2+ concentration ([Ca2+]i) and tension revealed that chloroethylclonidine pretreatment abolished the phenylephrine-induced increases in [Ca2+]i and tension in the Ca2+-free solution. The application of 5-methylurapidil (3 nM) to the chloroethylclonidine-pretreated strips completely inhibited the 3 μM phenylephrine-induced [Ca2+]i and tension increase in normal PSS. We concluded that both α1A- and α1B-adrenoceptors mediate the phenylephrine-induced contraction of the porcine renal artery accompanied by an increase in [Ca2+]i, and that α1A-adrenoceptors cause Ca2+ influx whereas α1B-adrenoceptors mainly mediate Ca2+ release.