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Pharmacology · Drugs acting on cholinergic synapses

Ganglionic Blockers

Ganglioplegica

Ganglionic blockers (drugs blocking N-cholinergic receptors) are a group of agents that interrupt signal transmission in autonomic ganglia. By inducing a state of "pharmacological denervation", they cause marked vasodilation and lower blood pressure, but due to a lack of selectivity, they are associated with a wide spectrum of adverse reactions.

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Main targetN-cholinergic receptors of sympathetic and parasympathetic ganglia
HemodynamicsDilation of veins and arteries, sharp drop in blood pressure
Main riskOrthostatic collapse (sudden drop in BP upon standing)
DurationFrom 10–20 minutes (in surgery) up to 3 hours (crisis management)
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Mechanism of action and target localization

Ganglionic blockers disrupt nerve impulse conduction from preganglionic to postganglionic fibers of the autonomic nervous system.

Main drug targets:

  • N-cholinergic receptors of autonomic ganglion neurons (both sympathetic and parasympathetic).
  • Chromaffin cells of the adrenal medulla — blockade of receptors in this area leads to a decrease in the release of endogenous catecholamines (adrenaline and noradrenaline), which additionally enhances the vasodilatory effect.
  • Carotid bodies — elimination of reflex excitation of the respiratory and vasomotor centers.

Effects on the cardiovascular system

The key pathogenetic mechanism in cardiology is the removal of the sympathetic nervous system's stimulatory influence on the heart and vascular bed.

Due to the blockade of sympathetic ganglia, the following hemodynamic changes are observed:

  1. Decrease in arterial tone and an overall drop in blood pressure (BP).
  2. Dilation of venous vessels, leading to blood pooling and a decrease in venous return.
  3. Decrease in venous pressure and stroke volume of the heart.

Important: a sharp drop in blood pressure often provokes reflex tachycardia and carries a high risk of orthostatic collapse.

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Effects of parasympathetic ganglion blockade

Since these drugs are non-selective, they also shut down the parasympathetic system, causing numerous adverse effects:

  • Vision: cycloplegia occurs (impaired near vision). Meanwhile, mydriasis (pupillary dilation) is less pronounced than with M-cholinergic blockers.
  • Heart: increased heart rate (tachycardia).
  • Smooth muscle: marked decrease in the tone of the gastrointestinal tract (GIT) and urinary bladder.
  • Secretion: suppression of salivary gland function (dry mouth — xerostomia), as well as bronchial, gastric, and intestinal glands.

Unlike M-cholinergic blockers, ganglionic blockers do not significantly affect bronchial tone.

Indications for use and classification

Due to numerous side effects, ganglionic blockers have completely lost their significance as maintenance drugs for arterial hypertension. Today, they are used only situationally.

1. Emergency management: Medium-duration agents (acting for 2.5–3 hours) are used — azamethonium bromide (pentamine) and hexamethonium (benzohexonium). Indications:

  • Hypertensive crises.
  • Pulmonary edema associated with high BP.
  • Peripheral arterial spasm.

2. Surgical practice ("controlled hypotension"): Short-acting ganglionic blockers (duration 10–20 minutes) administered via intravenous infusion are used — trimethafhan camsylate (arfonad) and trepirium iodide (hygronium). Goals:

  • Reduction of bleeding in the surgical field.
  • Prevention of cerebral edema during neurosurgical interventions.
  • Blockade of unwanted reflex vascular and cardiac responses during anesthesia.

Side effects and contraindications

Long-term use of these drugs is impossible due to severe complications. The main hazard is orthostatic hypotension up to profound fainting, associated with blood pooling in dilated veins. For prevention, the patient must strictly maintain bed rest for 1.5–2 hours post-injection.

Severe conditions can develop in the GI tract and urinary system: constipation, paralytic ileus (intestinal obstruction), and acute urinary retention.

Strict contraindications:

  • Severe hypotension, hypovolemia, and shock.
  • Acute myocardial infarction.
  • Severe hepatic and renal failure.
  • Angle-closure glaucoma (mydriasis blocks the anterior chamber angle, disrupting aqueous humor outflow and leading to a spike in intraocular pressure).
  • Prostatic hyperplasia (due to the risk of urinary retention).
  • Tendency to thrombosis (pressure drop causes blood stasis and promotes thrombosis).

Management of complications and overdose

Treatment strategy depends on the predominant symptom complex:

  • Intestinal or bladder atony: administration of M-cholinomimetics (aceclidine) or anticholinesterase agents (neostigmine bromide) is indicated.
  • Severe hypotension: $\alpha$-adrenergic agonists are used to increase vascular tone and raise blood pressure.
  • Respiratory depression: analeptic agents are indicated in case of ganglionic blocker overdose.

Class and exam questions

Why are ganglion blockers no longer used for chronic hypertension treatment?

These drugs cause total blockade of both sympathetic and parasympathetic ganglia. Lack of selectivity leads to severe side effects: cycloplegia, orthostatic collapse, intestinal obstruction, and urinary retention.

Why is the "controlled hypotension" technique used in surgery?

Artificially lowering blood pressure with short-acting ganglionic blockers drastically reduces bleeding in the surgical field and prevents cerebral edema, especially during neurosurgical operations.

What is the main rule for a patient after administration of a ganglion blocker?

The patient must remain in a supine position for 1.5–2 hours post-injection. This is necessary to prevent the development of orthostatic hypotension and syncopal episodes (fainting).

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What else to study on this topic

  • Chemical classification of ganglionic blockers (quaternary ammonium, sulfonium, and tertiary amines)
  • Pharmacodynamics of trimethaphan and trepirium iodide in anesthesiology
  • Differences between ganglionic blockers and M-cholinergic blockers: why their effects on bronchial tone differ
  • Mechanism of paralytic ileus development during parasympathetic ganglion blockade
  • Pathogenesis of intraocular pressure elevation in angle-closure glaucoma

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