G Protein control of inositol lipids in intact vascular smooth muscle

AbstractAgonist-induced PIP2, breakdown has been demonstrated in penneabilized vascular smooth muscle and shown to depend on a G protein. Segments of rat tail artery were permeabilized with ATP and EGTA after prelabeling with [3H]inositol. Norepinephrine and GTPγS were both able to increase levels of IP, IP2, and IP3 in the segments. The effects of both norepinephrine and GTPγS on the segments was non-additive. Aluminum fluoride also increased inositol phosphates in intact segments and norepinephrine-stimulated increases in IP, IP2, and IP3 were insensitive to pertussis toxin