Inositol trisphosphate angiotensin

I Kojima, H Shibata, E Ogata. (1986). Pertussis toxin blocks angiotensin II-induced calcium influx but not inositol trisphosphate production in adrenal glomerulosa cell. FEBS Lett 204 347-351. 

The same basic biochemical control mechanism causes contraction of the smooth muscle as well as secretion of aldosterone. The binding of angiotensin to its receptor activates a membrane phospholipase-C. It catalyses the hydrolysis of phosphoinositide phosphatidylinositol bis-phosphate to produce the two intracellular messengers, inositol trisphosphate (IP3) and diacylglycerol (DAG). 

JD Johnson, JC Garrison. (1987). Epidermal growth factor and angiotensin II stimulates formation of inositol 1,4,5 and inositol 1,3,4-trisphosphate in hepatocytes. J Biol Chem 262 17285-17293. 

Fig. 5.2 Early G-protein signaling events at the AT]R. Phospholipases C and D are sequentially activated by heterotrimeric G-protein subunits to produce important second messengers such as IP3 and DAG. See text for details. ATiR, angiotensin II type 1 receptor DAG, diacylglycerol IP3, inositol 1,4,5-trisphosphate PA, phosphatidic acid PC, phosphatidylcholine PIP2, phosphatidylinositol-4,5-bisphosphate PKC, protein kinase C PLC, phospholipase C PLD, phospholipase D.

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