The effect of insulin on potassium metabolism was examined in 29 healthy volunteers employing the insulin clamp technique with graded doses of insulin in combination with the hepatic venous catheter technique. The plasma insulin concentration was acutely raised and maintained at 27 ± 4, 51 ±6, 100 ±7, 428 ± 37, or 1 191 ± 12 μU/ml, whereas the plasma glucose concentration was held constant at the basal level by a variable glucose infusion. A dose-related decline in plasma potassium concentration was observed that varied between 0.58 ± 0.12 and 1.54 ± 0.23 meq/liter. During the 1st h of the insulin infusion, a marked increase in splanchnic potassium uptake occurred and accounted for approximately 70% of the decline in extracellular fluid potassium content. Splanchnic potassium uptake showed a positive correlation (r = 0,864, P < 0.001) with the decrease in plasma potassium concentration. During the 2nd h after insulin, splanchnic potassium balance returned to or below basal levels and an inverse correlation (r = -0.555, P < 0.05) between the fall in plasma potassium and net splanchnic balance was observed. In virtually all patients in whom the plasma potassium fell more than 1 meq/liter below basal, a net splanchnic efflux of potassium was observed during the 2nd h. When a simultaneous infusion of potassium chloride was given with insulin to prevent hypokalemia, splanchnic potassium balance remained markedly positive throughout the 2-h study. The decline in plasma potassium concentration was closely correlated with both the plasma insulin concentration and the total amount of glucose metabolized. In contrast, net splanchnic potassium balance showed no significant relationship to net glucose uptake by the splanchnic bed. We conclude the following. 1) Insulin causes a dose-related decline in the plasma potassium concentration that is progressive with time. 2) During the 1st h after insulin administration, the majority of the decline in plasma potassium concentration can be accounted for by net splanchnic potassium uptake. However, during the 2nd h after insulin, splanchnic potassium balance returns to or below basal levels, and peripheral tissues are primarily responsible for the continued fall in plasma potassium concentration. 3) Hypokalemia contributes, at least in part, to the reversal in net splanchnic potassium balance observed after 1 h of insulin infusion. 4) Insulin-mediated splanchnic potassium uptake is not dependent on net splanchnic glucose uptake.
|Original language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Physiology (medical)