Expression and function of α1-adrenoceptor subtypes in the porcine renal artery
| Autor: | Hiroshi Seguchi, Yinbi Zhou, Junji Nishimura, Katsuya Hirano, Hideo Kanaide |
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| Rok vydání: | 1998 |
| Předmět: |
Male
medicine.medical_specialty Contraction (grammar) Swine medicine.medical_treatment Molecular Sequence Data Gene Expression Biology Clonidine Phenylephrine chemistry.chemical_compound Renal Artery Chloroethylclonidine Receptors Adrenergic alpha-1 Internal medicine medicine.artery medicine Animals Amino Acid Sequence RNA Messenger Renal artery Antihypotensive agent Adrenergic alpha-Antagonists Pharmacology Base Sequence Antagonist Endocrinology chemistry Adrenergic alpha-1 Receptor Antagonists Calcium Female medicine.symptom Adrenergic alpha-Agonists Vasoconstriction Muscle Contraction medicine.drug Muscle contraction |
| Zdroj: | European Journal of Pharmacology. 341:95-103 |
| ISSN: | 0014-2999 |
| Popis: | We investigated the expression and function of alpha1-adrenoceptor subtypes in the porcine renal artery. Reverse transcription polymerase chain reaction (RT-PCR) and nucleotide sequencing indicated that the mRNAs for alpha1a- and alpha1b-adrenoceptors were expressed in the porcine renal artery. Chloroethylclonidine, an alpha1B- and alpha1D-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]dec ane-7,9-dione dihydrochloride), an alpha1D-adrenoceptor antagonist, had no effect. In contrast, 5-methylurapidil, an alpha1A-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 microM phenylephrine-induced [Ca2+]i and tension increase in normal PSS. We concluded that both alpha1A- and alpha1B-adrenoceptors mediate the phenylephrine-induced contraction of the porcine renal artery accompanied by an increase in [Ca2+]i, and that alpha1A-adrenoceptors cause Ca2+ influx whereas alpha1B-adrenoceptors mainly mediate Ca2+ release. |
| Databáze: | OpenAIRE |
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