Bethanidine hydriodide
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Bethanidine hydriodide is an orally active antihypertensive agent and adrenergic neuron blocker. Bethanidine hydriodide exerts its antihypertensive effect by inhibiting the release of norepinephrine from sympathetic nerve terminals. Bethanidine hydriodide exhibits anti-ventricular arrhythmic activity. Bethanidine hydriodide can be used in research related to hypertension, ventricular tachycardia, and ventricular fibrillation.
For research use only. We do not sell to patients.
- CAS No.: 2863-34-5
- Formula: C10H16IN3
- Molecular Weight:305.16
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Storage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
In Vitro
Bethanidine hydriodide (1-3 μg/mL) abolishes the inhibitory effect of neural stimulation on the pendular movement of isolated rabbit ileum[1].
Bethanidine hydriodide (1-10 μg/mL) attenuates the neurostimulatory contractile response of isolated guinea pig vas deferens at a concentration of 1 μg/mL, and completely abolishes this response at 3 μg/mL[1].
Bethanidine hydriodide (3-300 μg/mL) inhibits the peristaltic reflex of isolated guinea pig ileum; it reduces cholinergic sensitivity at concentrations of 3 to 30 μg/mL, and decreases the sensitivity to acetylcholine and histamine by 10-fold at a concentration of 300 μg/mL[1].
Bethanidine hydriodide (100-300 μg/mL) inhibits serotonin-induced contraction of isolated rat uterus and adrenaline-induced contraction of isolated rabbit uterus[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Bethanidine hydriodide (0.3-100 mg/kg; intravenous/oral administration) induces dose-dependent pressor effects, adrenergic neuron blockade, and enhanced amine responses in dogs, and exhibits good tolerance to high oral doses[1].
Bethanidine hydriodide (10 mg/kg; subcutaneous injection) transiently slows gastrointestinal transit in fasted rats, and an accelerated transit rate is observed 4 h after administration[1].
Bethanidine hydriodide reduces motor activity in mice at high doses. When administered intravenously at 12.5 mg/kg, it prolongs pentobarbital-induced hypnotic duration, and exhibits route-dependent toxicity, with an LD50 of 12 mg/kg for intravenous injection and 520 mg/kg for oral administration[1].
Bethanidine hydriodide (300 mg/kg) increases the ventricular fibrillation threshold by 150% in the hearts of normal dogs and by 327% in the hearts of infarcted dogs, with no acute toxicity observed even at doses as high as 300 mg/kg[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Cat (anaesthetized with chloralose, pentobarbitone, or nitrous oxide; unanaesthetized)[1]
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Dosage:0.1-30 mg/kg (i.v.); 0.5-100 mg/kg (s.c.); 1.25-5 mg/kg (p.o.)
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Administration:i.v.; s.c.; p.o.
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Result:Caused a blood pressure fall of 20-60 mmHg lasting over 1 hour at 0.3 or 1 mg/kg i.v..
Raised blood pressure by 20-50 mmHg with tachycardia lasting 10 minutes at additional 1 mg/kg i.v..
Decreased hind limb vasoconstrictor responses to sympathetic chain stimulation at 0.1-0.5 mg/kg i.v..
Abolished hind limb vasoconstrictor responses to sympathetic chain stimulation and reversed nerve stimulation to increase blood flow at 1 mg/kg i.v..
Decreased pressor responses to 200 μg tyramine at 3-10 mg/kg.
Abolished nictitating membrane contractions to pre- or post-ganglionic sympathetic nerve stimulation, while increased responses to adrenaline and noradrenaline.
Caused nictitating membrane contractions ≤30% of maximum at 3-10 mg/kg i.v..
Partially relaxed the nictitating membrane at 1.25 mg/kg s.c. or p.o..
Fully relaxed the nictitating membrane with effects persisting 2-3 days at 2.5 mg/kg s.c. or p.o..
Impaired preganglionic nerve responses at 24 hours at 1 mg/kg s.c. or p.o..
Abolished preganglionic nerve responses at 3 mg/kg s.c. or p.o..
Almost abolished spleen contractions to splenic nerve stimulation 30 minutes after 0.3 mg/kg i.v..
Reduced noradrenaline release from the spleen during nerve stimulation to 1/10 of control levels 15 minutes after 0.3 mg/kg i.v..
Abolished rapid pressor responses to splanchnic nerve stimulation or dimethylphenylpiperazinium in adrenalectomized cats for over 1 hour at 0.3-0.5 mg/kg i.v..
Abolished piloerection for at least 30 minutes at 0.5 mg/kg i.v..
Reduced sweat secretion for 10-15 minutes at 3-10 mg/kg i.v..
Did not reduce pressor amine content of cat irises at 24 hours at single subcutaneous doses of 3, 10, or 30 mg/kg.
Caused respiratory paralysis and neuromuscular block of gastrocnemius muscle response to indirect stimulation at 10-20 mg/kg i.v..
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Animal Model:Albino mice[1]
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Dosage:/
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Administration:i.v.; i.p.; p.o.; s.c.
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Result:Did not change motor activity at 50 mg/kg p.o..
Decreased motor activity at 50 mg/kg i.p. and 200 mg/kg p.o..
Prolonged pentobarbitone hypnosis at 12.5 mg/kg i.v..
Did not prolong pentobarbitone hypnosis at 6.25 mg/kg i.v..
Had LD50 values of 12 mg/kg (i.v.), 150 mg/kg (i.p.), 260 mg/kg (s.c.), 520 mg/kg (p.o.).
Chemical Information
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CAS No. 2863-34-5
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Appearance Solid
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Molecular Weight 305.16
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Formula C10H16IN3
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SMILES
CN/C(NC)=N/CC1=CC=CC=C1.I
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
[1]. BOURA AL, et al. Adrenergic neurone blockade and other acute effects caused by N-benzyl-N'N"-dimethylguanidine and its ortho-chloro derivative. Br J Pharmacol Chemother. 1963;20(1):36-55. [Content Brief]
[2]. Bacaner MB, et al. Antiarrhythmic, antifibrillatory, and hemodynamic actions of bethanidine sulfate: an orally effective analog of bretylium for suppression of ventricular tachyarrhythmias. Am J Cardiol. 1982;50(4):728-734. [Content Brief]
[3]. Gifford RW. Bethanidine sulfate—a new antihypertensive agent. JAMa. 1965 Sep 13;193(11):901-5.
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bethanidine hydriodide Related Classifications
HY-16094A Related Classifications
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