(+)-Norfenfluramine a major hepatic metabolite of (+)-fenfluramine, is a selective 5-HT2B receptor agonist (Ki: 11.2 nM). (+)-Norfenfluramine potently stimulates the hydrolysis of inositol phosphates and increases intracellular Ca2+. (+)-Norfenfluramine can be used for the research of primary pulmonary hypertension and valvular heart disease[1].
(+)-Norfenfluramine (1 nM to 100 μM) contracts arteries with a dramatic decrease in threshold (aorta and mesenteric resistance artery) in rats[1].
(+)-Norfenfluramine (1 and 10 μM, 3 min) induces contraction in aorta from tissues of normotensive and hypertensive rats[1].
(+)-Norfenfluramine (0-10 μM, 3 min) induces 5-HT release from rat hippocampal synaptosomes by Ca2+-dependent way [2].
(+)-Norfenfluramine (1-300 μg/kg, i.v.) induces pressor response in conscious SHAM and DOCA-salt rats[1].
(+)-Norfenfluramine (2.5 and 5 mg/kg, i.p.) decreases of 5-HT and 5-HIAA levels in telencephalon and brainstem of rats[3].
| Animal Model: | Conscious SHAM and DOCA-salt rats[1]. |
| Dosage: | 1-300 μg/kg |
| Administration: | Intravenous injection (i.v.), given in a cumulative fashion at 6-min intervals. |
| Result: | Induced pressor response in conscious SHAM and DOCA-salt rats. (change in mean arterial blood pressure at 300 μg/kg, mm Hg, SHAM vehicle=36, SHAM ketanserin=7, DOCA=51, DOCA ketanserin=19). |
[1]. Wei Ni, et al. The 5-hydroxytryptamine2A receptor is involved in (+)-norfenfluramine-induced arterial contraction and blood pressure increase in deoxycorticosterone acetate-salt hypertension. J Pharmacol Exp Ther. 2007 May;321(2):485-91.
[2]. M Gobbi, et al. In vitro studies on the mechanism by which (+)-norfenfluramine induces serotonin and dopamine release from the vesicular storage pool. Naunyn Schmiedebergs Arch Pharmacol. 1998 Sep;358(3):323-7.
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