**Core Concept**
Suxamethonium, a depolarizing muscle relaxant, works by mimicking the action of acetylcholine at the neuromuscular junction, leading to sustained depolarization and muscle paralysis. This results from its ability to bind to nicotinic acetylcholine receptors (nAChRs) at the motor endplate.

**Why the Correct Answer is Right**
Suxamethonium's mechanism of action is centered around its potentiation of acetylcholine's effects on nAChRs, causing the rapid influx of sodium ions, which leads to muscle contraction and eventually paralysis. This action is mediated by the receptor's specific subunits, particularly the alpha subunit, which is essential for the binding of suxamethonium.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because suxamethonium does indeed cause muscle fasciculations, which are transient, involuntary muscle contractions, as a result of its initial depolarizing effect on the motor endplate.

**Option B:** This option is incorrect because suxamethonium is known to cause an increase in end-tidal CO2, a consequence of the muscle paralysis and subsequent respiratory muscle weakness.

**Option C:** This option is incorrect because suxamethonium can cause anaphylactoid reactions, which are severe, life-threatening allergic reactions that can occur within minutes of administration.

**Clinical Pearl / High-Yield Fact**
A notable side effect of suxamethonium is its potential to cause hyperkalemia, particularly in patients with denervated muscles, such as those with spinal cord injuries or burns. This is due to the release of potassium ions from the muscle cells.

**Correct Answer: D.**