Not a single trial — a mechanistic reference chart. This audit checks each cell against standard pharmacology sources and flags where the one-page version oversimplifies.
Every X in the original grid checks out against standard pharmacology references.
| Agent | B1 | B2 | A1 | Na+ | K+ | NO↑ |
|---|---|---|---|---|---|---|
| Metoprolol | ✓ | |||||
| Atenolol | ✓ | |||||
| Bisoprolol | ✓ | |||||
| Propranolol | ✓ | ✓ | ✓ | |||
| Nadolol | ✓ | ✓ | ||||
| Sotalol | ✓ | ✓ | ✓ | |||
| Carvedilol | ✓ | ✓ | ✓ | mild | ||
| Labetalol | ✓ | ✓ | ✓ | mild | ||
| Nebivolol | ✓ | ✓↑ |
The mechanism column in the original post is correct; here's the physiologic reasoning underneath it.
| Blocked | Why it produces that effect |
|---|---|
| B1 | B1 receptors are the dominant cardiac subtype; blocking them reduces cAMP-driven calcium influx in the SA node, AV node, and myocardium — slower rate, weaker contraction, slower conduction. |
| B2 | B2 receptors mediate smooth-muscle relaxation in bronchi and skeletal-muscle vasculature; blocking them removes that relaxation, which is why non-selective agents carry bronchospasm risk in reactive airway disease and can blunt the adrenergic warning signs of hypoglycemia. |
| A1 | Alpha-1 blockade removes peripheral arterial and venous vasoconstriction, dropping afterload directly — this is the mechanism that gives carvedilol and labetalol an added BP-lowering effect beyond what B1 blockade alone provides. |
| Na+ | Also called membrane-stabilizing activity (MSA): high-dose blockade of fast sodium channels slows phase-0 depolarization, widening the QRS. Clinically most relevant in beta-blocker overdose, where propranolol's combined B1/Na+ blockade makes it disproportionately dangerous compared with cardioselective agents. |
| K+ | Sotalol's potassium-channel blockade is its defining class III antiarrhythmic property (this is why it's dosed and monitored differently from other beta blockers) — it prolongs the QT interval, which is therapeutic for reentrant arrhythmias but is also the mechanism behind sotalol's dose-dependent torsades risk. |
| NO↑ | Nebivolol stimulates endothelial nitric oxide release, producing vasodilation independent of beta blockade — the mechanism behind its comparatively neutral hemodynamic and metabolic profile relative to older agents. |
Nothing here is wrong. These are the dose- and context-dependencies a single grid can't show.
Metoprolol, atenolol, and bisoprolol are B1-selective at typical therapeutic doses, but that selectivity narrows and eventually disappears at higher doses — a "cardioselective" agent can still provoke bronchospasm in a severe asthmatic at high enough dosing. The chart's clean X-in-a-box format necessarily can't carry a dose-response curve.
The vasodilatory, NO-mediated benefit is most prominent at the doses where B1 selectivity holds; at higher doses nebivolol loses selectivity and the NO-release advantage is correspondingly less clinically distinct from other agents.
The chart correctly labels their A1 effect "mild" rather than a full checkmark — worth noting for bedside use: this is exactly why both are reasonable choices when you want beta blockade plus some afterload reduction without the more pronounced orthostatic hypotension risk of a dedicated alpha blocker.
This is an accurate, well-constructed reference chart. Every receptor assignment matches standard pharmacology teaching, and the two-column format (blocked receptor / mechanism when blocked) is a genuinely efficient way to hold this much information on one page. The additions above are context a static grid structurally can't carry — dose-dependence of selectivity, and the clinical stakes of the Na+ and K+ columns specifically in overdose and arrhythmia management, respectively.