Betahistine dihydrochloride is an anti-vertigo drug. It was first registered in Europe in 1970 for the treatment of Ménière's disease. It is commonly prescribed to patients with balance disorders or to alleviate vertigo symptoms associated with Ménière's disease.
Pharmacokinetics
Betahistine comes in both a tablet form as well as an oral solution, and is taken orally. It is rapidly and completely absorbed. The mean plasma half-life is 3–4 hours, and excretion is virtually complete in the urine within 24 hours. Plasma protein binding is very low. Betahistine is transformed into aminoethylpyridine and hydroxyethylpyridine and excreted with the urine as pyridylacetic acid. There is some evidence that one of these metabolites, aminoethylpyridine, may be active and exert effects similar to those of betahistine on ampullar receptors.
Mode of action
Betahistine has a very strong affinity as an antagonist for histamine H3 receptors and a weak affinity as an agonist for histamine H1 receptors. Betahistine seems to dilate the blood vessels within the inner ear which can relieve pressure from excess fluid and act on the smooth muscle.
Betahistine has two modes of action. Primarily, it has a direct stimulating (agonistic) effect on H1 receptors located on blood vessels in the inner ear. This gives rise to local vasodilation and increased permeability, which helps to reverse the underlying problem of endolymphatic hydrops.
More importantly, betahistine has a powerful antagonistic effects at H3 receptors, thereby increasing the levels of neurotransmitters histamine, acetylcholine, norepinephrine, and serotonin released from the nerve endings. The increased amounts of histamine released from histaminergic nerve endings can stimulate receptors. This stimulation explains the potent vasodilatory effects of betahistine in the inner ear, that are well documented.
from:Acridine Raw Material
Pharmacokinetics
Betahistine comes in both a tablet form as well as an oral solution, and is taken orally. It is rapidly and completely absorbed. The mean plasma half-life is 3–4 hours, and excretion is virtually complete in the urine within 24 hours. Plasma protein binding is very low. Betahistine is transformed into aminoethylpyridine and hydroxyethylpyridine and excreted with the urine as pyridylacetic acid. There is some evidence that one of these metabolites, aminoethylpyridine, may be active and exert effects similar to those of betahistine on ampullar receptors.
Mode of action
Betahistine has a very strong affinity as an antagonist for histamine H3 receptors and a weak affinity as an agonist for histamine H1 receptors. Betahistine seems to dilate the blood vessels within the inner ear which can relieve pressure from excess fluid and act on the smooth muscle.
Betahistine has two modes of action. Primarily, it has a direct stimulating (agonistic) effect on H1 receptors located on blood vessels in the inner ear. This gives rise to local vasodilation and increased permeability, which helps to reverse the underlying problem of endolymphatic hydrops.
More importantly, betahistine has a powerful antagonistic effects at H3 receptors, thereby increasing the levels of neurotransmitters histamine, acetylcholine, norepinephrine, and serotonin released from the nerve endings. The increased amounts of histamine released from histaminergic nerve endings can stimulate receptors. This stimulation explains the potent vasodilatory effects of betahistine in the inner ear, that are well documented.
from:Acridine Raw Material
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