Changes in luminal flow rate modulate basal and bradykinin-stimulated cell [Ca2+] in aortic endothelium
✍ Scribed by Juan A. Oliver; Herbert S. Chase Jr.
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 491 KB
- Volume
- 151
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Hemodynamic forces influence many endothelial cell functions. The coupling between hemodynamic forces and cell function could be mediated by mechano‐sensitive ion channels present in the plasma membrane of endothelial cells. Because one of these channels is permeable to Ca^2+^, we tested whether hemodynamic forces influence endothelial cell Ca^2+^ ([Ca^2+^]~i~). Bovine aortic endothelial cells were grown inside cylindrical glass tubes, loaded with fura‐2, and perfused at different pressures and flow rates on the stage of a fluorescence microscope. Decreasing flow from 110 to 2 ml.min^−1^ raised [Ca^2+^]~i~ from 57 ± 11 to 186 ± 29 nM (mean ± SEM, p < 0.01) by increasing the entry of extracellular Ca^2+^ into the cytoplasm. Increasing flow from 2 to 110 ml.min^−1^ transiently decreased [Ca^2+^]~i~ from 62 ± 3 to 33 ± 5 nM (p < 0.01) apparently due to reduced Ca^2+^ entry and concomitant extrusion by the plasma membrane Ca^2+^‐ATPase. The rise in [Ca^2+^]~i~ induced by bradykinin was magnified during a decrease in flow; in control cells, 10^−7^ M bradykinin increased [Ca^2+^]~i~ by 162 ± 26 nM, whereas [Ca^2+^]~i~ increased 350 ± 67 nM (p < 0.05) in cells previously exposed to 110 ml.min^−1^. These observations suggest that flow‐induced changes in [Ca^2+^]~i~ might be a signal‐transduction mechanism for endothelial functions responsive to hemodynamic forces and may also modulate the magnitude of hormonally mediated increases in [Ca^2+^]~i~. © 1992 Wiley‐Liss, Inc.