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Hypertension. 2001;38:709-712

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(Hypertension. 2001;38:709.)
© 2001 American Heart Association, Inc.


Obesity- and Diabetes-Related Hypertension

Relation of Cellular Potassium to Other Mineral Ions in Hypertension and Diabetes

Lawrence M. Resnick; Mario Barbagallo; Ligia J. Dominguez; Joseph M. Veniero; J. P. Nicholson; Raj K. Gupta

From the Hypertension Center, New York Presbyterian Hospital-Cornell Medical Center (L.M.R., M.B., J.P.N.), New York, New York; Institute of Internal Medicine and Geriatrics, University of Palermo (M.B., L.J.D.), Palermo, Italy; and Department of Physiology and Biophisics, Albert Einstein College of Medicine (J.M.V., R.K.G.), Bronx, New York.

Correspondence to Lawrence M. Resnick, MD, Hypertension Center, New York Presbyterian Hospital-Cornell Medical Center, 525 E 68th St, Starr 4 Pavillon, New York, NY 10021.

Abstract

Abstract— To investigate the role of intracellular potassium (Ki)and other ions in hypertension and diabetes, we utilized 39K-, 23Na-, 31P-, and 19F-nuclear magnetic resonance (NMR) spectroscopy to measure Ki, intracellular sodium (Nai), intracellular free magnesium (Mgi), and cytosolic free calcium (Cai), 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 (Ki=148±2.0 mmol/L), Ki 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). Ki 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 Ki and Nai values, saline infusion elevated Nai (P<0.01) and reciprocally suppressed Ki levels (142±2.4 to 131±2.2 mmol/L, P<0.01). Ki was strongly and inversely related to Cai (r=-0.846, P<0.001), and was directly related to Mgi (r=0.664, P<0.001). We conclude that (1) Ki depletion is a common feature of essential hypertension and type 2 diabetes, (2) treatment of hypertension at least partially restores Ki levels toward normal, and (3) fasting steady-state Ki levels are closely linked to Cai and Mgi 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.


Key Words: potassium • diabetes • calcium • magnetic resonance spectroscopy • hypertension




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