Modulation of K channels by coexpressed human alpha1C-adrenoceptor in Xenopus oocytes
Autor: | Gea-Ny Tseng, J. Tseng-Crank, J. A. Yao |
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Rok vydání: | 1997 |
Předmět: |
Chronotropic
medicine.medical_specialty Potassium Channels Time Factors Transcription Genetic Calmodulin Physiology Xenopus Stimulation Biology Membrane Potentials Phenylephrine Xenopus laevis Downregulation and upregulation Receptors Adrenergic alpha-1 Physiology (medical) Internal medicine Phorbol Esters medicine Animals Humans Protein kinase A Receptor biology.organism_classification Recombinant Proteins Cell biology Kinetics Endocrinology Oocytes biology.protein Tetradecanoylphorbol Acetate Female Signal transduction Cardiology and Cardiovascular Medicine |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 272:H1275-H1286 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.1997.272.3.h1275 |
Popis: | alpha1-Adrenoceptors participate in the regulation of inotropy and chronotropy in the heart. Modulation of cardiac K-channel function plays an important role in these alpha1-adrenergic functions. Studies of the mechanisms of K-channel modulation by alpha1-adrenoceptors are hampered by the coexistence of multiple receptor and channel subtypes in the heart. We therefore used a model system of coexpressing a specific receptor (human alpha1c-adrenoceptor) and a K-channel clone (hIsK, rKv1.2, or rKv1.4) in oocytes. alpha1c-Adrenoceptor stimulation caused a rapid upregulation of hIsK by elevating the intracellular Ca concentration. At least part of this effect was due to an activation of calmodulin and Ca/calmodulin-dependent protein kinase II. On the other hand, alpha1c-adrenoceptor stimulation caused a slow downregulation of rKv1.2 and rKvl.4 by activating protein kinase C. The differential modulation of K channels by alpha1c-adrenoceptors demonstrated in our experiments corroborates the complexity of alpha1-adrenergic functions in the heart. Our results indicate that the oocyte model system can be a useful approach in studying alpha1-adrenergic modulation of ion-channel function and signal transduction. |
Databáze: | OpenAIRE |
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