Hypertension, Vol 7, 447-451, Copyright © 1985 by American Heart Association
RW Alexander, TA Brock, MA Gimbrone Jr and SE Rittenhouse
Angiotensin II stimulated the breakdown of phosphatidylinositol-4,5-
bisphosphate (PIP2) and the generation of inositol trisphosphate (IP3) in
cultured rat aortic smooth muscle cells. The decrease in PIP2 and increase
in IP3 levels were rapid (measurable at 5 seconds; maximum IP3 levels at 15
seconds). The time course of these changes was comparable to that of
angiotensin II-induced increases in cytosolic free calcium, as measured by
the calcium-sensitive fluorescent indicator quin 2. The IP3 formation was
not stimulated by the calcium ionophore A23187 (5 microM), nor were
angiotensin II-induced changes in IP3 formation inhibited by the removal of
extracellular calcium with EGTA. Angiotensin II appears to be capable of
generating more IP3 than is required for maximal release of intracellular
calcium. These data are consistent with the hypothesis that generation of
IP3 plays a role in the angiotensin II-induced mobilization of calcium from
intracellular storage sites in vascular smooth muscle cells.
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Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle
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