Final answer:
B-adrenergic agents interact with beta-adrenergic receptors to activate a cascade that increases cAMP, thereby potentially decreasing extracellular K+ levels by promoting its uptake into cells. B-blockers would inhibit this effect, possibly leading to higher plasma potassium levels.
Step-by-step explanation:
The effect of B-adrenergic agents on plasma K+ (potassium ions) involves their interaction with beta-adrenergic receptors, which are coupled to Gs proteins. These receptors, when stimulated, activate a cascade that leads to an increased concentration of the second messenger cyclic AMP (cAMP). The elevation of cAMP through the activation of protein kinase A (PKA) results in several intracellular responses, including the phosphorylation of proteins that modulate the activity of ion channels.
While the pharmacology of B-adrenergic agents is complex and varied, generally speaking, the activation of B-adrenergic receptors can lead to an influx of K+ from the extracellular space into cells. This occurs because B-adrenergic agonists induce the activation of Na+/K+-ATPase pumps, which increase potassium uptake into skeletal muscle cells, thereby lowering extracellular potassium levels. In contrast, B-adrenergic antagonists, like β-blockers, would counteract this effect by inhibiting the B-adrenergic receptors, potentially leading to higher plasma potassium levels.