It's important to keep in mind that extracellular potassium concentration is normally very tightly regulated at 4.2 mEq/L (±0.3 mEq/L in nonpathological circumstances.) It's precisely because so many cells are so sensitive to extracellular potassium levels.
Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. [Emphasis mine.]
If this were the case, the entire body would need respond to increased K+ levels, which would present some difficulties. So your second interpretation is the correct one.
Or does this mean that the stimulation causes a direct intake of potassium ions FROM THE PLASMA INTO THE CARDIAC CELLS, hence causing a less negative membrane potential and an easier firing of an action potential?
The effect of receptor stimulation is localized to the cells which have that receptor. So β-adrenergic receptor stimulation causes in increase in heart rate and contractility, whereas β blockers decreases same.
One of my mnemonics for β-adrenergic receptors was "1 heart, 2 lungs" to remind me that the heart was predominantly β1 and the lungs β2.