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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00486.2001
Submitted on October 12, 2001
Accepted on February 20, 2002
1 Physiology, UTSW, Dallas, TX, USA
* To whom correspondence should be addressed. E-mail: hligeman{at}utsw.swmed.edu.
Phosphatidylinositol-4,5 bis phosphate (PIP2) affects profoundly several cardiac ion channels and transporters, but very little is known about its regulation in the heart. Recordings of PIP2-sensitive currents in excised patches suggest that sarcolemmal PIP2 can be rapidly synthesized and broken down via ATP- and calcium (Ca2+)-dependent processes, respectively, for the most part within 30 s. To test when, and if, total PIP and PIP2 levels actually change in intact heart, we used a new non-radioactive, HPLC method to quantify anionic phospholipids. In superfused atria and arterially perfused ventricles of guinea pigs, total PIP and PIP2 levels (10-30 µmol/Kg wet weight) do not change, or even increase, with activation of G
(q)/phospholipase C (PLC)-dependent pathways by carbachol (50 µM), phenylephrine (50 µM), and endothelin-1 (0.3 µM). The PLC inhibitor, U73122 (20 µM), is without effect in atrium. Adenosine (0.2 mM) and phorbol 12-myristate 13-acetate (PMA, 1µM) both cause approximately 30% reduction of PIP2 in ventricles, suggesting that a diacylglycerol (DAG)-dependent mechanism negatively regulates cardiac PIP2. DAG analogues cause similar PIP2 reductions in a mouse kidney cortical collecting tubule (M1) cell line, but cause an increase of PIP2 in other cell lines. PIP2, but not PIP, increases reversibly by 30% during electrical stimulation (2 Hz for 5 min) in guinea pig left atria; the increase is blocked by nickel (2 mM), and similar effects occur in guinea pig and frog ventricles. Both PIP and PIP2 increase within 3 min in hypertonic solutions, roughly in proportion to osmolarity, and similar effects occur in 4 cell lines. Inhibitors of several volume-sensitive signaling mechanisms do not affect these responses, suggesting that PIP2 metabolism might be sensitive to membrane tension, per se. Together, these results verify that PIP2 is turning over within one to, at most, a few minutes in intact heart. Cardiac PIP2 seems rather insensitive to hormone-dependent activation of PLC's; it is sensitive to molecular processes involved in the activation of contraction and to changes of cell volume; it appears to be negatively regulated by a DAG-dependent mechanism.
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