Bradykinin-stimulated calcium influx in cultured bovine aortic endothelial cells
Autor: | S. G. Eskin, William P. Schilling, L. T. Navarro, A. K. Ritchie |
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Rok vydání: | 1988 |
Předmět: |
Fura-2
Physiology Bradykinin chemistry.chemical_element Calcium chemistry.chemical_compound Cytosol Physiology (medical) Extracellular Animals Aorta Calcimycin Cells Cultured Benzofurans Calcium metabolism Chemistry Nitrendipine Membrane transport Rubidium Endothelial stem cell Kinetics Biochemistry Biophysics Cattle Endothelium Vascular Cardiology and Cardiovascular Medicine |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 255:H219-H227 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.1988.255.2.h219 |
Popis: | Bradykinin (BK)-stimulated release of endothelium-derived relaxing factor has been linked to a rise in cytosolic Ca2+ concentration and a change of K+ permeability of the endothelial cell. In the present study, measurement of BK-induced changes in fura-2 fluorescence and 86Rb+ efflux were used to monitor changes in cytosolic Ca2+ and K+ permeability in cultured bovine aortic endothelial cells. In the presence of normal extracellular Ca2+, BK induced a fourfold increase in cytosolic Ca2+, which peaked at 20 s and declined within 1 min to a value that was 50% of the peak level. Subsequently, cytosolic Ca2+ decreased and approached basal levels within 8 min. In the absence of Ca2+, BK produced a 1.5- to 2-fold increase in cytosolic Ca2+ that peaked within 20 s and declined to basal levels within 2 min. Addition of Ca2+ to the Ca-free reaction buffer 3-5 min after addition of BK resulted in a two-to threefold increase in cytosolic Ca2+ that declined slowly back to basal levels. Thus Ca2+ influx can occur in response to BK at a time when there is minimal elevation of cytosolic Ca2+ above the resting level. Under all conditions tested, 86Rb+ efflux paralleled changes in the cytosolic Ca2+, suggesting that efflux occurred through Ca2+-activated K+ channels. Isosmotic substitution of Na+ with N-methyl-D-glucamine did not affect the BK-stimulated changes in cytosolic Ca2+ or 86Rb+ efflux, suggesting that Na+-Ca2+ exchange plays little role in the BK response. These results suggest that BK stimulates Ca2+ influx via a BK receptor-operated channel or a channel activated by some internal messenger other than Ca2+. |
Databáze: | OpenAIRE |
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