Abstract
The interaction of hormones, growth factors, or cytokines to their specific cell surface receptors can lead to the stimulation of a cascade of biochemical events including the activation of several phospholipases which in turn can result in the release of several lipid second messengers (1) as outlined. Thus, the action of angiotensin II (AII) or other vascular smooth muscle cell (VSMC) growth factors can activate one or more phospholipases, phosphoinositide phospholipase C (PI-PLC), phosphatidylcholine-specific PLC (PC-PLC), or phospholipase D (PLD). This process results in the formation of the second messengers inositol trisphosphate (IP3), which leads to calcium (Ca2+) mobilization from intracellular stores, as well as diacylglycerol (DAG) which in turn can activate the Ca2+- and phospholipid-sensitive protein kinase C (PKC) (2-5). It has been suggested that the cellular response to AII is obtained by the temporal integration of the IP3/Ca2+-calmodulin branch responsible for the initial transient response and the DAG/PKC branch responsible for the sustained phase of All action (6). DAG is also a rich source of AA that can be released by the action of the enzyme DAG lipase (7) whereas the enzyme DAG-kinase can convert DAG to phosphatidic acid.
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Natarajan, R., Stern, N., Nadler, J. (1996). Arachidonic Acid Metabolites on Renin and Vascular Smooth Muscle Cell Growth. In: Sowers, J.R. (eds) Endocrinology of the Vasculature. Contemporary Endocrinology, vol 1. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0231-8_26
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DOI: https://doi.org/10.1007/978-1-4612-0231-8_26
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