In healthy older participants, the magnitude of the fall in systolic blood pressure and increase in heart rate induced by intraduodenal glucose are attenuated when the exposure of glucose to the small intestinal mucosa and subsequent glucose absorption is slowed by guar.

Background: Potassium (K⁺) input occurs after meals or during ischemic exercise and is accompanied by a high concentration of L-lactate in plasma (P_L-lactate). Methods: We examined whether infusing 100 µmol L-lactic acid/min for 15 min would lead to a fall in the arterial plasma K⁺ concentration (P_K). We also aimed to evaluate the mechanisms involved in normal rats compared with rats with acute hyperkalemia caused by a shift of K⁺ from cells or a positive K⁺ balance. Results: There was a significant fall in P_K in normal rats (0.25 mM) and a larger fall in P_K in both models of acute hyperkalemia (0.6 mM) when the P_L-lactate rose. The arterial P_K increased by 0.8 mM (p < 0.05) 7 min after stopping this infusion despite a 2-fold rise in the concentration of insulin in arterial plasma (P_Insulin). There was a significant uptake of K⁺ by the liver, but not by skeletal muscle. In rats pretreated with somatostatin, P_Insulin was low and infusing L-lactic acid failed to lower the P_K. Conclusions: A rise in the P_L-lactate in portal venous blood led to a fall in the P_K and insulin was permissive. Absorption of glucose by the Na⁺-linked glucose transporter permits enterocytes to produce enough ADP to augment aerobic glycolysis, raising the P_L-lactate in the portal vein to prevent postprandial hyperkalemia.