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. β2 stimulation in the lungs decreases smooth muscle contractility, which is why we used to give epinephrine to those with asthma attacks. That's been replaced with albuterol and atropine, but epi is still useful if the attack is severe enough.