How does the SNS increase the heart rate when it causes an increase in cellular uptake of potassium?

Question

Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. Thus, a more negative membrane voltage will arise as the potassium ions flow out of the cardiac muscle cells more easily due to the more steep ionic gradient set.

This, consequently, makes it more difficult for an action potential to fire, and as a result, a decrease in the heart rate. So now since the sympathetic nervous system increases the heart rate, then why does this beta adrenergic stimulation occur? It would decrease the heart rate, so what is happening?

This information is from the medical physiology Guyton and Hall textbook, page 384, put into my own words if I have understood it correctly. This is the entire quote from it:

"β-Adrenergic Stimulation Increases Cellular Uptake of Potassium: Increased secretion of catecholamines, especially epinephrine, can cause movement of potassium from the extracellular to the intracellular fluid, mainly by activation of β2-adrenergic receptors." 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?

Many thanks in advance!

Answer 1

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.

More than I knew and more than you probably want to know at this point abot about β-adrenergic receptors in the heart

_{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.}