Related Experiment Video
Updated: Jan 19, 2026

Simultaneous Measurements of Intracellular Calcium and Membrane Potential in Freshly Isolated and Intact Mouse Cerebral Endothelium
Published on: January 20, 2019
Effects of changes in extra- and intracellular K+ on the endothelial production of prostacyclin
1Institute of Interdisciplinary Research, School of Medicine, Free University of Brussels, Belgium.
Abstract:
1. Changes in the KCl concentration of the incubation medium, from 0 to 80 mM, had no effect on the basal or ATP-stimulated release of prostacyclin (PGI2) from bovine aortic endothelial cells. 2. The monovalent cation ionophores, valinomycin and nigericin (5 microM), enhanced the release of PGI2 from endothelial cells stimulated by ATP or bradykinin. 3. The action of nigericin, unlike that of valinomycin, was time-dependent, abolished in a high-KCl medium and associated with an increased efflux of 86Rb and a time-dependent depletion of intracellular K+. 4. Ouabain (1-100 microM) also enhanced the release of PGI2 in response to ATP and induced a significant depletion of intracellular K+ in bovine aortic endothelial cells. 5. In conclusion, modifications of the endothelial cell membrane potential, resulting from changes in the extracellular K+ concentration, do not modulate the basal or ATP-stimulated production of PGI2. An acute depletion of intracellular K+ by nigericin or ouabain enhances the production of PGI2 in aortic endothelial cells stimulated by ATP or bradykinin.
More Related Videos
Related Concept Videos
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Regulation of Angiogenesis and Blood Supply
Intracellular Signaling Affects Focal Adhesions
Some...
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
Nitric Oxide Signaling Pathway
Clot Retraction and Fibrinolysis
![Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production](/_next/image?url=https%3A%2F%2Fcloudfront.jove.com%2FCDNSource%2Fteasers%2F54014.jpg&w=3840&q=50)
