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style="background: #F8EABA; text-align: center;" colspan="2" Hexamethonium
CAS number
PubChem 3604
Molecular formula C12H30N22+
Molar mass 202.38
style="background: #F8EABA; text-align: center;" colspan="2" Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references

Hexamethonium is a ganglionic blocker,[1] a neuronal nAch (NN) receptor antagonist which acts in autonomic ganglia by binding mostly in or on the NN receptor, and not the acetylcholine binding site itself. It has no effect on 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.

Pharmacology[edit | edit source]

It can act on receptors at pre-ganglionic sites in both the sympathetic and parasympathetic nervous system, which are both regulated (again, only pre-ganglionically) by nicotinic acetylcholine receptors. Postganglionic sympathetic systems are usually regulated by norepinephrine or adrenaline (adrenergic receptors), while parasympathetic systems are still acetylcholine based, but 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.

Uses[edit | edit source]

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 hexamethonium, an unapproved drug, in a normal volunteer during a medical study is believed to have caused her death.[3][4]

See also[edit | edit source]

References[edit | edit source]

  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.
  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?. URL accessed on 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.

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