Atrial natriuretic peptide increases glucose uptake during hypoxia in cardiomyocytes.

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.