EXPRESSION AND FUNCTION OF ALPHA(1)-ADRENOCEPTOR SUBTYPES IN THE PORCINE RENAL-ARTERY

We investigated the expression and function of alpha(1)-adrenoceptor s ubtypes in the porcine renal artery. Reverse transcription polymerase chain reaction (RT-PCR) and nucleotide sequencing indicated that the m RNAs for alpha(1a)-and alpha(1b)-adrenoceptors were expressed in the c ontraction, while 3 nM BMY 7378 piperazinyl]ethyl]-8-azaspiro[4.5]deca ne-7,9-dione dihydrochloride), an alpha(1D)-adrenoceptor antagonist, h ad no effect. In contrast, 5-methylurapidil, an alpha(1A)-adrenoceptor antagonist, induced a rightward shift of the phenylephrine concentrat ion-response curve. The simultaneous measurement of cytosolic Ca2+ con centration ([Ca2+],) and tension revealed that chloroethylclonidine pr etreatment abolished the phenylephrine-induced increases in [Ca2+], an d tension in the Ca2+-free solution. The application of 5-methylurapid il (3 nM) to the chloroethylclonidine-pretreated strips completely inh ibited the 3 mu M phenylephrine-induced [Ca2+](i) and tension increase in normal PSS. We concluded that both alpha(1A)-and alpha(1B)-adrenoc eptors mediate the phenylephrine-induced contraction of the porcine re nal artery accompanied by an increase in [Ca2+](i), and that alpha(1A) -adrenoceptors cause Ca2+ influx whereas alpha(1B)-adrenoceptors mainl y mediate Ca2+ release. (C) 1998 Elsevier Science B.V.