Magnesium effects in rabbit ventricle.

Ten to twenty millimoles per liter Mg did not affect 42-K exchange in control isolated blood-perfused rabbit septa, but abolished acetyl strophanthidin (ACS)-induced net 42-K loss (constant heart rate) without attenuating the mechanical response. In six septa ACS-induced net K loss was reduced from 159.3 plus or minus 45 to 43.5 plus or minus 35 mumol/kg tissue water (P smaller than 0.05) by increasing Mg from 1.0 to 20 mM without a change in inotropic response. Ten to twenty millimoles per liter Mg did not reverse ACS inhibition of 42-K5 tissue uptake. In eight septa 16 mM K doubled the efflux rate for 42-K in 1mM Mg. Twenty millimoles per liter Mg abolished this effect. Sixteen millimoles per liter K increase 42-K effluent counts by 99.5 plus or minus 18.5 percent of control in 1.0 mM Mg, but by 44.9 plus or minus 14.1 percent (P smaller than 0.001) in 20 mM Mg. Mg inhibited 42-K exchange at sites that became rate limiting after ACS treatment. These sites were activated by 16mM K. ACS inotrophy was not quantitatively related to net K loss. The Mg effect during digitalis exposure did not result from reversal of ACS inhibition of NA-K-ATPase activity but from a separate effect on K efflux.