Key result
A 30-day potassium-deficient diet in rats increased myocardial alpha-1 density (62 to 148 fmols/mg) and epinephrine arrhythmia duration (56 to 224 s), reversing after 5 days of normal diet.
Why the study?
Does a potassium-deficient diet increase myocardial adrenergic receptor densities and epinephrine arrhythmogenicity in adult laboratory rats?
Does a potassium-deficient diet increase myocardial adrenergic receptor densities and epinephrine arrhythmogenicity in adult laboratory rats?
Prolonged potassium restriction in rats increases myocardial alpha-1 and beta receptor densities and epinephrine arrhythmogenicity, which are reversible with normal potassium intake.
Hypothesis-generating for hypokalemia-induced arrhythmogenicity; leaves open translation to human potassium management.
We studied the effects of a 30-day potassium (K+)-deficient diet on blood [K+] myocardial adrenergic receptor densities, serum catecholamines, and epinephrine arrhythmogenicity in adult laboratory rats (250 +/- 25 g). Within 3 days of beginning the K+-deficient diet, blood [K+] decreased by 50%. After 5 days, the myocardial alpha-1 density increased (62 +/- 2 vs 148 +/- 16 fmols/mg protein), and the total beta receptor increased (95 +/- 5 vs 273 +/- 49) without significant change in receptor affinity. However, 18-21 days of this diet was necessary to produce an increase in the duration of epinephrine arrhythmias (from 56 +/- 8 to 224 +/- 21 s). While prazosin block of the alpha-1 receptor in hypokalemic rats caused a significant, 42% reduction in arrhythmic duration and propranolol block caused a 62% reduction, both prazosin and propranolol were necessary to return arrhythmia times to normal (44 +/- 0.3 mmols/dL). Total serum catecholamines were reduced after 3 days of the diet (from 482 +/- 37 to 299 +/- 31 pg/ml) and remained depressed throughout the 30 days of the K+ diet. The results of this study indicate that prolonged restriction causes a reduction in serum catecholamines, an increase in myocardial alpha-1 and beta receptors densities, and an increase in epinephrine arrhythmogenicity. All of these changes were reversed within 5 days of initiating a normal dietary K+ intake.
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Miletich et al. (1997) studied Hypokalemia. Potassium (K+)-deficient diet vs. Normal dietary K+ intake / baseline was evaluated on Myocardial adrenergic receptor densities, serum catecholamines, and epinephrine arrhythmogenicity. A 30-day potassium-deficient diet in rats increased myocardial alpha-1 density (62 to 148 fmols/mg) and epinephrine arrhythmia duration (56 to 224 s), reversing after 5 days of normal diet.
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