1. In incubated tubule fragments from renal cortex of fed rats gluconeogenesis from pyruvate was stimulated by adrenaline (1μm optimum) and by the selective α-adrenergic agonists oxymetazoline and amidephrine. The selective β-agonists isoproterenol and salbutamol were ineffective at concentrations up to 10μm. 2. Stimulation of gluconeogenesis by 1μm-adrenaline was almost completely blocked by 10μm-phentolamine (α-antagonist), partially blocked by 10μm-phenoxybenzamine (α-antagonist) and unaffected by 10μm-propranolol (β-antagonist). 3. Adrenaline stimulation of gluconeogenesis was rapid and was sustained for at least 1h. 4. Oxymetazoline (α-agonist) was extremely potent in stimulation of gluconeogenesis. This compound stimulated glucose production from pyruvate, lactate and glutamate, but not from succinate or glycerol. 5. In the absence of Ca2+ oxymetazoline was ineffective, whereas some stimulatory effect of adrenaline on gluconeogenesis was still observed. 6. Glucagon had no effect on gluconeogenesis from pyruvate in the presence of 1.27mm-Ca2+ and inhibited the process in the presence of 0.25mm-Ca2+. Parathyrin (parathyroid hormone) stimulated gluconeogenesis at 1.27mm-Ca2+. 7. In short incubations of tubule fragments glucagon, papaverine and adrenaline significantly increased 3′:5′-cyclic AMP. Adrenaline also slightly decreased 3′:5′-cyclic GMP. Oxymetazoline had no effect on the amount of either cyclic nucleotide. 8. At all concentrations tested, theophylline and papaverine decreased gluconeogenesis from pyruvate. 9. It is concluded that renal gluconeogenesis may be increased by α- but not β-adrenergic stimuli and that this is probably independent of changes in 3′:5′-cyclic AMP or 3′:5′-cyclic GMP. An involvement of Ca2+ in the action of oxymetazoline appears likely, but this is less certain with adrenaline.

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