Autoregulation of renal hemodynamics is not impaired by a 'physiologic' dose of glucagon

Glucagon has been suggested to be involved in the pathway by which protein and amino acids elevate renal blood flow (RBF) and glomerular filtration rate (GFR) postprandially. Recent data suggest that amino acids elevate RBF and GFR through an autoregulatory mechanism (i.e., by impairing renal autoregulation). If glucagon mediates the renal hemodynamic effects of amino acids, 'physiologic' infusion of glucagon would also be expected to impair autoregulation. We examined the effects of glucagon (5 ng/kg per min given intraportally and intravenously) on RBF and GFR autoregulation in anesthetized dogs. Intraportal glucagon (n = 6) increased RBF (24%) and GFR (23%) at normal arterial pressure. RBF and GFR were well autoregulated (greater than 90% of control) at renal arterial pressures greater than or equal to 85 mm Hg before and after glucagon. At 70 mm Hg, RBF and GFR decreased by 15 and 16%, respectively, before glucagon and by 19 and 22%, respectively, after glucagon. Intravenous glucagon (n = 6) produced similar effects. Intraportal glucagon at 500 ng/kg per min increased RBF (35%), heart rate (69%) and plasma glucose (78%) and decreased arterial pressure (16%) (GFR not measured). This dose impaired RBF autoregulation by 30%. The data suggest that a 'physiologic' dose of glucagon increases renal hemodynamics without impairing renal autoregulation. It is suggested that glucagon's vasodilatory effect on the renal vasculature may be additive to the renal effects of amino acids.