title: Atrial natriuretic peptide increases glucose uptake during hypoxia in cardiomyocytes.
abstract: The action of atrial natriuretic peptide on glucose uptake during hypoxia was investigated in neonatal cardiomyocytes. When the cultures were exposed to 100 n and 1 and 10 micro M of atrial natriuretic peptide for 60 min, hypoxia-induced glucose uptake significantly increased from 20.4 +/- 1.2 to 28.2 +/- 3.1, 31.6 +/- 2.7, and 30.1 +/- 2.8 pmol/h/mg protein, respectively, although atrial natriuretic peptide alone did not significantly affect the basal glucose uptake in normoxic condition. The atrial natriuretic peptide-stimulated glucose uptake during hypoxia was significantly decreased by 100 n of genistein and tyrphostin A-23 (a tyrosine kinase inhibitor) from 31.6 +/- 2.7 to 22.8 +/- 2.4 and 23.8 +/- 2.7 pmol/h/mg protein. U73122 100 n, which is a phospholipase C antagonist, significantly inhibited the atrial natriuretic peptide-induced glucose uptake under hypoxic conditions from 31.6 +/- 2.7 to 13.6 +/- 1.9 pmol/h/mg protein. However, the atrial natriuretic peptide-induced glucose uptake did not involve elevation of intracellular Ca and phosphatidylinositol (PI)3 kinase. It was concluded that the atrial natriuretic peptide-stimulated glucose uptake during hypoxia acts through a phospholipase C-tyrosine kinase pathway.
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism / Q000494:pharmacology*; D015687:Cell Hypoxia / Q000187:drug effects* / Q000502:physiology; D002478:Cells, Cultured; D005947:Glucose / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D051381:Rats
chemical_list: D009320:Atrial Natriuretic Factor; D005947:Glucose