Abstract
Endothelin-1 (ET-1) is released from endothelial cells (EC) following gene activation of preproET mRNA and the subsequent proteolytic processing into biologically active peptide [1]. ET-1 activates ETB receptors on EC, promoting the release of endothelium-derived relaxing factor (EDRF), and ETA and ETB receptors on vascular smooth muscle cells (VSMC), promoting events coupled to both vasoconstriction and growth [2]. Activation of ETA/ETB receptors by ET-1 results in activation of the effector enzyme, phospholipase C (PLC) through a Gq-coupled receptor with the subsequent production of the hydrolytic products 1,4,5 inositol-trisphosphate (IP3) and diacylglycerol (DAG) [2]. These mediators subsequently promote [Ca2+]i release from sarcoplasmic reticulum (SR) stores and activate protein kinase C (PKC) respectively.
Keywords
- Human Vascular Smooth Muscle Cell
- Bucca Versus
- Mesangial Cell Growth
- Gopalakrishnan Versus
- preproET mRNA
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Hopfner, R.L., McNeill, J.R., Gopalakrishnan, V. (2001). Interactions between the ACE and the endothelin pathway. In: D’Orléans-Juste, P., Plante, G.E. (eds) ACE Inhibitors. Milestones in Drug Therapy MDT. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-7579-0_4
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