Pharmacodynamics<unk>  is a strong antagonist of the histamine H3 receptor and a weak agonist of the histamine H1 receptor.<unk>  has two mechanisms of action. Primarily, it is a weak agonist on the 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,<unk>  has a powerful antagonistic effects at H3 receptors, thereby increasing the levels of neurotransmitters histamine, acetylcholine, norepinephrine, serotonin, and GABA 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<unk>  in the inner ear, that are well documented.<unk>  seems to dilate the blood vessels within the inner ear which can relieve pressure from excess fluid and act on the smooth muscle. It is postulated that<unk> 's increase in the level of serotonin in the brainstem inhibits the activity of vestibular nuclei. Pharmacokinetics<unk>  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 elimination half-life is 3 to 4 hours, and excretion is virtually complete in the urine within 24 hours. Plasma protein binding is very low.<unk>  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<unk>  on ampullar receptors.
Betahistine
Allergan
Methacholine
Caffeine
Dihydroergotamine
Theobromine
Histamine dihydrochloride
Antihistamine