Elevation of arterial potassium during acute systemic hypoxia is abolished by alkalosis

Abstract

Background: Small elevations in plasma potassium evoke vasodilation in the peripheral circulation. Systemic hypoxia elevates arterial potassium and also modifies arterial pH. Aims: We examined the interaction between pH and potassium in blood during systemic hypoxia and the effect of pH on the uptake/release of potassium in the peripheral tissues. Methods: Anesthetized dogs were ventilated with air plus oxygen for normoxia or air plus nitrogen for hypoxia. Some animals received intravenous sodium bicarbonate to elevate pH by 0.1 units. Arterial plasma potassium concentration was measured in normoxia and hypoxia. A rat gracilis muscle was perfused with normoxic Krebs buffer and the potassium content of the venous outflow was compared during perfusion at pH 7.4, 6.8, or 7.8. Results: In dogs with an arterial pH of 7.40-7.45, systemic hypoxia elevated the arterial potassium by 1 mmol/L. An arterial pH of 7.55 did not alter the basal potassium concentration, but it abolished the hypoxia-induced increase. In rat muscle, reduction of the perfusate pH from 7.4 to 6.8 reduced arterial perfusion pressure from 8.73 to 7.32 kPa and venous potassium from 6.6 to 5.2 mM. Elevation of perfusate pH to 7.8 decreased the arterial perfusion pressure from 8.44 to 6.95 kPa but did not affect venous potassium. Conclusions: The hypoxia-induced elevation of arterial potassium is abolished by increasing the pH to 7.55. This is not due to enhanced potassium uptake into peripheral tissues at high pH. Red blood cells are suggested as the most likely source of the potassium released in hypoxia.