Effects of glucagon, insulin, propionate, acetate, and HCO3 on K excretion in sheep

Abstract

The effects on renal K excretion of 1 h intravenous infusion of glucagon, insulin, Na propionate, Na acetate, or NaHCO3 were studied in mature, conscious fasted ewes. These treatments were compared with the fasted state without treatment (control) and with feeding a single daily meal. Renal K excretion was increased by feeding and by Na propionate and Na acetate treatments but not by infusion of glucagon, insulin, and NaHCO3. Since hormone levels were elevated more by specific hormone infusions than by feeding or Na propionate infusions, these results do not support a role for glucagon and insulin in mediating the increases in renal K excretion that occurred after meals or during acetate and propionate infusions. The mechanisms responsible for the acetate- and propionate-induced kaliuresis are not clear but do not appear to include changes in plasma K (PK), glucagon, and insulin (Pinsulin) or in urine flow and urine Na excretion. However, a relation between insulin and K was observed during infusion of KCl in fasting sheep. Above a PK threshold of 4 meq/l, Pinsulin (ng/ml) = 1.52 PK (meq/l) - 5.89. In other experiments, K excretion increased after an intravenous bolus injection of 1 mg of glucagon, indicating that sheep, like humans and dogs, respond to pharmacologic doses of glucagon with kaliuresis.

NaHCO3 and KHCO3 ingestion rapidly increases renal electrolyte excretion in humans

“…In contrast, the fractional excretion of K ϩ progressively increased over time, peaking at 71 Ϯ 12% of the filtered load at 270 min, consistent with the peak effects of aldosterone occurring 1-2 h after it increases (12,41). These results are consistent with previous studies of K ϩ loading in humans (9,30,37,38) and other animals (3,6,7,21,32,41). It is likely that elevated plasma [K ϩ ] and aldosterone concentration independently contributed to the kaliuresis (9, 31) by increasing principal cell Na ϩ -K ϩ -ATPase activity (34) and intracellular [K ϩ ] in the distal tubule and cortical collecting duct (13,15).…”