The mechanisms and significance of the coupled release of endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) from endothelial cells.
Endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) are co-released from endothelial cells by stimuli acting via membrane-bound receptors or via non-receptor mediated mechanisms. The receptor-mediated release of EDRF and PGI2 is calcium-dependent and seems to be under the negative feedback regulation of protein kinase C. Significant interactions between EDRF and PGI2 or between their respective second messengers within the endothelial cell have not yet been conclusively demonstrated. Furthermore, although EDRF and PGI2 synergize in the inhibition of platelet aggregation, there is little evidence for such synergism in smooth muscle relaxation. These observations indicate that EDRF and PGI2 release may be coupled primarily by their requirement for raised intracellular calcium levels and by their regulation through protein kinase C.
Department of Pharmacology, Faculty of Medical Sciences, UNICAMP, Campinas, Brazil.
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Hyslop
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de Nucci
D000818:Animals; D002118:Calcium / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D011464:Epoprostenol / Q000378:metabolism*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism*; D010974:Platelet Aggregation / Q000502:physiology; D013927:Thrombosis / Q000097:blood*
D009569:Nitric Oxide; D011464:Epoprostenol; D002118:Calcium