Potassium depletion (KD) is a very common clinical entity often associated with adverse cardiac effects. KD is generally considered to reduce muscular Na-K-ATPase density and secondarily reduce K uptake capacity. In KD rats we evaluated myocardial Na-K-ATPase density, ion content, and myocardial K reuptake. KD for 2 wk reduced plasma K to 1.8 ± 0.1 vs. 3.5 ± 0.2 mM in controls ( P < 0.01, n = 7), myocardial K to 80 ± 1 vs. 86 ± 1 μmol/g wet wt ( P < 0.05, n = 7), increased Mg, and induced a tendency to increased Na. Myocardial Na-K-ATPase α2-subunit abundance was reduced by ∼30%, whereas increases in α1- and K-dependent pNPPase activity of 24% ( n = 6) and 13% ( n = 6), respectively, were seen. This indicates an overall upregulation of the myocardial Na-K pump pool. KD rats tolerated a higher intravenous KCl dose. KCl infusion until animals died increased myocardial K by 34% in KD rats and 18% in controls ( P < 0.05, n = 6 for both) but did not induce different net K uptake rates between groups. However, clamping plasma K at ∼5.5 mM by KCl infusion caused a higher net K uptake rate in KD rats (0.22 ± 0.04 vs. 0.10 ± 0.03 μmol·g wet wt−1·min−1; P < 0.05, n = 8). In conclusion, a minor KD-induced decrease in myocardial K increased Na-K pump density and in vivo increased K tolerance and net myocardial K uptake rate during K repletion. Thus the heart is protected from major K losses and accumulates considerable amounts of K during exposure to high plasma K. This is of clinical interest, because a therapeutically induced rise in myocardial K may affect contractility and impulse generation-propagation and may attenuate increased myocardial Na, the hallmark of heart failure.
Transient Amino-aciduria in Severe Potassium Depletion