['Insulin and epinephrine stimulate glucose uptake through distinct mechanisms. We tested the hypothesis that the golgi apparatus is involved in insulin-stimulated but not epinephrine-stimulated glucose transport and phosphorylation.', 'We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-(3)H]glucose (5 mmol/l, 0.05 microCi/ml) and Na-oleate (0.4 mmol/l). In the absence or presence of the inhibitor of golgi function, brefeldin A (30 micromol/l), either insulin (1 mU/ml), epinephrine (1 micromol/l), or phenylephrine (100 micromol/l) plus propranolol (10 micromol/l, selective alpha -adrenergic stimulation) were added to the perfusate.', 'Cardiac power was stable in all groups (between 8.56+/-0.61 and 10.4+/-1.11 mW) and increased (34%) with addition of epinephrine, but not with selective alpha -adrenergic stimulation. Insulin, epinephrine, and selective alpha -receptor stimulation increased glucose transport and phosphorylation (micromol/min/g dry wt, basal: 1.19+/-0.13, insulin: 3.89+/-0.36, epinephrine: 3.46+/-0.27, alpha -stimulation: 4.08+/-0.40). Brefeldin A increased basal glucose transport and phosphorylation and blunted insulin-stimulated but not epinephrine-stimulated glucose transport and phosphorylation. Selective alpha -stimulated glucose transport and phosphorylation was also blunted by brefeldin A.'] Is insulin-stimulated glucose transport dependent on Golgi function in isolated working rat heart?