Relation of cellular potassium to other mineral ions in hypertension and diabetes

To investigate the role of intracellular potassium (K-i)and other ions in hypertension and diabetes, we utilized K-39-, Na-23-, P-31-, and F-19-nuclear magnetic resonance (NMR) spectroscopy to measure K-i, intracellular sodium (Na-i), intracellular free magnesium (Mg-i), and cytosolic free calcium (Ca-i), respectively, in red blood cells of fasting normotensive nondiabetic control subjects (n = 10), untreated (n = 13) and treated (n = 14) essential hypertensive subjects, and diabetic subjects (n = 5). In 12 subjects (6 hypertensive and 6 normotensive controls), ions were also measured before and after the acute infusion of 1 L of normal saline. Compared with those in controls (K-i = 148 +/- 2.0 mmol/L), K-i levels were significantly lower in hypertensive (132.2 +/- 2.9 mmol/L, sig = 0.05) and in type 2 diabetic subjects (121.2 +/- 6.8 mmol/L, sig = 0.05). K-i was higher in treated hypertensives than in untreated hypertensives (139 +/- 3.1 mmol/L, sig = 0.05) but was still lower than in normals. Although no significant relation was observed between basal K-i and Na-i values, saline infusion elevated Na-i (P <0.01) and reciprocally suppressed K-i levels (142 +/- 2.4 to 131 +/- 2.2 mmol/L, P <0.01). K-i was strongly and inversely related to Ca-i (r = -0.846, P <0.001), and was directly related to Mg-i (r = 0.664, P <0.001). We conclude that (1) K-i depletion is a common feature of essential hypertension and type 2 diabetes, (2) treatment of hypertension at least partially restores K-i levels toward normal, and (3) fasting steady-state K-i levels are closely linked to Ca-i and Mg-i homeostasis. Altogether, these results emphasize the similar and coordinate nature of ionic defects in diabetes and hypertension and suggest that their interpretation requires an understanding of their interaction.