Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.

Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic activity, ion channels remain closed, blocking neuromuscular transmission and causing muscle relaxation.

The antagonistic effect can be overcome by increasing acetylcholine concentration using acetylcholinesterase (AChE) inhibitors. Elevated acetylcholine displaces the blocker, restoring neuromuscular transmission. However, the blockers can directly block Na⁺ channels at high doses, resulting in irreversible neuromuscular blockade unresponsive to AChE inhibitors.