Effect of intravenous glucagon infusion on renal haemodynamics and renal tubular handling of sodium in healthy humans

Abstract

Schwartz Sørensen S, Eiskjær H, ørskov H, Bjerregaard Pedersen E. Effect of intravenous glucagon infusion on renal haemodynamics and renal tubular handling of sodium in healthy humans. Scand J Clin Lab Invest 1993; 53: 25-34.

The effects of a 2-h intravenous infusion of glucagon 5 ng kg⁻¹ min⁻¹ or placebo on glomerular filtration rate (GFR), renal plasma flow (RPF), tubular sodium handling as judged by the lithium clearance method, and plasma concentrations of angiotensin II (AngII), aldosterone (Aldo), and atrial natriuretic factor (ANF) were investigated in two groups of healthy human volunteers, glucagon group (n = 10), and placebo group (n = 10).

Glucagon infusion resulted in a maximal increase in plasma concentrations of glucagon of 400%. GFR increased 5.9% (range 1.3-12.4, p<0.001) through the whole infusion period, whereas RPF only increased transiently during the first hour of infusion 6.5% (range 2.6-15.3, p<0.05). Whereas filtered load of sodium increased significantly in response to glucagon infusion (p<0.001), urinary sodium excretion was unchanged. Neither of these variables were affected by placebo. As judged from assessments of tubular sodium handling derived from the renal clearance of lithium, the increased filtered load of sodium resulted in an increase in the output of sodium from the proximal tubules of a similar magnitude, and an increase in absolute reabsorption of sodium in the distal tubules totally counterbalancing this increased input to the distal tubules. These alterations in tubular sodium handling did not involve Ang II, Aldo, or ANF.

We conclude that an increase in plasma concentration of glucagon within the physiological range is capable of inducing a small and sustained increase in GFR, whereas RPF increases only transiently. Glucagon induces an increase in filtered load of sodium which is totally counter-balanced in the distal tubules resulting in unchanged urinary sodium excretion.

Key Words:

• aldosterone
• angiotensin II
• atrial natriuretic factor
• glomerular filtration rate
• glucagons
• lithium clearance
• renal haemodynamics
• sodium