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Hexamethonium: Wikis


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Systematic (IUPAC) name
CAS number 60-26-4
ATC code  ?
PubChem 3604
ChemSpider 3478
Chemical data
Formula C12H30N2
Mol. mass 202.38 g/mol
SMILES eMolecules & PubChem
Pharmacokinetic data
Bioavailability  ?
Metabolism  ?
Half life  ?
Excretion  ?
Therapeutic considerations
Pregnancy cat.  ?
Legal status
Routes  ?

Hexamethonium is a ganglionic blocker,[1] a neuronal nAch (NN) receptor antagonist that acts in autonomic ganglia by binding mostly in or on the NN receptor, and not the acetylcholine binding site itself. It has effect on neither the muscarinic acetylcholine receptors (mAChR) located on target organs of the parasympathetic nervous system nor the nicotinic acetylcholine receptors at the neuromuscular junction (NM) that are responsible for skeletal muscle motor response.



It can act on receptors at pre-ganglionic sites in both the sympathetic and parasympathetic nervous systems, which are both regulated (by nicotinic ligand-gated ionotropic acetylcholine receptors). Postganglionic sympathetic systems are usually regulated by norepinephrine or noradrenaline (adrenergic receptors), whereas parasympathetic systems are still acetylcholine-based, and instead rely on muscarinic receptors (some post-ganglionic sympathetic neurons, such as those stimulating sweating, release acetylcholine).

The organ system and adverse effects of ganglion blockers are because both the parasympathetic and sympathetic stimuli are blocked at the preganglionic sites. Side-effects include combined sympatholytic (e.g., orthostatic hypotension and sexual dysfunction) and parasympatholytic effects (e.g., constipation, urinary retention, glaucoma, blurry vision, decreased lacrymal secretion, dry mouth (xerostomia) effects.


It was formerly used to treat disorders of the peripheral nervous system, such as chronic hypertension, which is innervated only by the sympathetic nervous system. The non-specificity of this treatment led to discontinuing its use.[2]

The use of inhaled hexamethonium, an unapproved drug, in a normal volunteer during a medical study is believed to have caused her death. [3][4] Her lung tissue reportedly "had the appearance of ground glass."

See also


  1. ^ Sonoyama K, Tajima K, Fujiwara R, Kasai T (March 2000). "Intravenous infusion of hexamethonium and atropine but not propranolol diminishes apolipoprotein A-IV gene expression in rat ileum". The Journal of nutrition 130 (3): 637–41. PMID 10702597.  
  2. ^ Hardman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 10th edition, 2001, pp 210-211.
  3. ^ "Johns Hopkins’ Tragedy: Could Librarians Have Prevented a Death?". Retrieved 2008-10-06.  
  4. ^ Savulescu J, Spriggs M (February 2002). "The hexamethonium asthma study and the death of a normal volunteer in research". Journal of medical ethics 28 (1): 3–4. PMID 11834748. PMC 1733509.  


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