Discussion
heart failure, normokalemia, hypertension
HEART FAILURE, HYPERTENSION
In this study we showed an increase in TBK over a six-month period using dietary guidance, oral potassium supplements and MRAs in patients with normokalemia at baseline. Furthermore, changes in p-K did not reflect changes in TBK in a simple manner as p-K increased significantly over weeks and was attenuated over months of continued treatment, while TBK increased gradually over the six-month study period. The results indicate the time it takes to accumulate intracellular potassium.The observed increase in TBK was significantly larger than it would be, if only extracellular potassium levels were increased. Thus, in an adult, the total amount of potassium in the extracellular fluid is on average 50–75 mmol ~ 1,950–2,925 mg. The estimated increase in TBK found in the present study of 82 mg/kg corresponds to 158 mmol ~ 6,150 mg of potassium in a person weighing 75 kg, i.e., more than twice the total amount of potassium in the extracellular space. This, in combination with only a small increase in p-K, makes it is reasonable to conclude that the vast amount of the increase in TBK was accumulated intracellularly.No other trial has tested the effects of dietary guidance, potassium supplementation and MRAs on TBK, but a few earlier trials have investigated the effects of potassium supplementation when added to non-potassium sparing diuretics. In 1974, Dargie et al. studied groups of six to eight middle-aged patients and showed a non-significant reduction in TBK from 116.6 g (SD 11.4) to 115.8 g (SD 10.2) after four months when potassium supplements was given in combination with non-potassium sparing diuretics [Animal studies have shown a significantly larger increase in TBK [The present study is the first to demonstrate that TBK can be increased in normokalemic patients who are not treated with non-potassium sparing diuretics by administering lower doses of potassium supplements (average 36 mmol daily), when used in combination with dietary guidance and concomitant inhibition of the renal potassium loss by administration of MRAs. In addition, it is the first study to demonstrate the timing of changes in p-K and TBK.We observed a numerical increase in p-K of 0.16 mmol/l at the six months follow-up. This is consistent with increases in p-K of 0.16 to 0.30 mmol/l in patients with heart failure treated with MRA and with p-K increases of 0.09–0.19 mmol/l in patients with hypertension treated with potassium supplements [