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Phosphoinositides and Signal Transduction in the Cat Carotid Body

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The phosphoinositides, namely phosphatidylinositol-4,5-bisphosphate (PIP2) and phosphatidylinositol (PI) play an influential role in intracellular signaling. Phospholipase C (PLC) hydrolyzes PIP2 and PI to produce the signaling molecules inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) which act to mobilize intracellular calcium and to stimulate protein phosphorylation, respectively.1 Quantifying PLC changes is thus one way to assess the phosphoinositide-dependent signal transduction process. We have previously reported that there are measurable amounts of PLC activity in the cat carotid body in the normoxic condition and that PLC activity is increased by hypoxia.2 Since activation of PLC may be part of the general mechanism by which the carotid body stimuli induce physiologic effects, we now extended that study by characterization of the effects on phosphoinositide metabolism of two further natural carotid body stimuli, respiratory and metabolic acidosis.


  • Metabolic Acidosis
  • Carotid Body
  • Respiratory Acidosis
  • Signal Transduction Process
  • Phosphoinositide Metabolism

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© 1992 Springer Science+Business Media New York

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Pokorski, M., Strosznajder, R. (1992). Phosphoinositides and Signal Transduction in the Cat Carotid Body. In: Honda, Y., Miyamoto, Y., Konno, K., Widdicombe, J.G. (eds) Control of Breathing and Its Modeling Perspective. Springer, Boston, MA.

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