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STIMULATION OF PHOSPHATIDYLINOSITOL TURNOVER IN ADULT RAT LEFT ATRIA DOES NOT INVOLVE RELEASE OF INOSITOL (1,4,5) TRI SPHOSPHATE
Author(s) -
Anderson Karen E.,
Myers Damian,
Woodcock Elizabeth A.
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb01698.x
Subject(s) - inositol , phosphatidylinositol , stimulation , inositol phosphate , endocrinology , medicine , phosphate , chemistry , biology , biochemistry , receptor , signal transduction
SUMMARY 1. The turnover rate of inositol (1,4,5) tris phosphate (Ins(1,4,5)P 3 ) in noradrenaline‐stimulated adult rat left atria was calculated from changes in specific activity and was found to equal 110 ct/min per mg tissue. In contrast, the isomers of inositol mono‐ and bis phosphates accumulated at a rate of 508 ct/min per mg. 2. Neomycin, which inhibits release of Ins (1,4,5)P 3 , inhibited the accumulation of inositol phosphates in noradrenaline‐stimulated isolated neonatal cardiomyocytes but did not inhibit accumulation in left atria. 3. These data demonstrate that most of the inositol phosphates which accumulate in adult rat left atria do not derive from Ins (1,4,5) P 3 . 4. These data are best explained by a model in which noradrenaline stimulation results mainly in the breakdown of phosphatidylinositol(4) mono phosphate (PtIns(4)P 1 ) to inositol(1,4) bis phosphate (Ins(1, 4)P 2 ). Thus, heart tissue avoids the generation of Ins(1,4,5)P 3 .