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Selected Publication:
Graier, WF; Kukovetz, WR; Groschner, K.
Cyclic AMP enhances agonist-induced Ca2+ entry into endothelial cells by activation of potassium channels and membrane hyperpolarization.
Biochem J. 1993; 291 ( Pt 1)(6):263-267
Doi: 10.1042/bj2910263
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- Leading authors Med Uni Graz
- Graier Wolfgang
- Co-authors Med Uni Graz
- Groschner Klaus
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- Abstract:
- The mechanism underlying cyclic AMP (cAMP)-mediated amplification of agonist-induced Ca2+ responses in endothelial cells was investigated in pig endothelial cells. Forskolin, adenosine and isoprenaline, as well as the membrane-permeant cAMP analogue dibutyryl cAMP, enhanced bradykinin-induced rises in intracellular free Ca2+ as well as bradykinin-induced Mn2+ entry. These agents were also found to hyperpolarize endothelial cells without increasing intracellular Ca2+ by itself, i.e. in the absence of bradykinin. Both amplification of bradykinin effects and the hyperpolarizing action was blocked by the protein kinase inhibitor H-8. The involvement of K+ channels in the hyperpolarizing effects of forskolin was consequently studied in perforated outside-out vesicles. Two different types of K+ channels were recorded, one of which had a large conductance (170 pS) and was activated by forskolin. We suggest that stimulation of endothelial adenylate cyclase results in activation of large-conductance K+ channels and consequently in membrane hyperpolarization, which in turn enhances bradykinin-induced entry of Ca2+ by increasing its electrochemical gradient.
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- Action Potentials - drug effects
- Animals -
- Aorta -
- Bradykinin - pharmacology
- Bucladesine - pharmacology
- Calcium - metabolism Calcium - pharmacology
- Cell Membrane - drug effects Cell Membrane - physiology
- Cyclic AMP - metabolism Cyclic AMP - pharmacology
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- Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism
- Ethers, Cyclic - pharmacology
- Forskolin - pharmacology
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- Potassium Channels - drug effects Potassium Channels - physiology
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