Shown: posts 1 to 6 of 6. This is the beginning of the thread.
Posted by linkadge on June 15, 2007, at 18:21:54
As many of you may know I have been obsessed to death with the possability that SSRI and related medicinces may cause the same type of heart dammage that fenfluramine and the recently withdrawn dopamine agonists with 5-ht2b agonism.
Apparently a metabolite of trazodone, mcpp is a potent 5-ht2b agonist. I think this med may be related to similar problems.
The following is a link to an article that I need to read, as it directly relates to my concerns, but I do not have the required membership.
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1601-5215.2007.00195.x
Does anyone have Larry Hoover's email adress? You can babblemail it to me, he won't mind as he has given it to me before.
Linkadge
Posted by linkadge on June 15, 2007, at 18:30:37
In reply to The end of Trazodone?, posted by linkadge on June 15, 2007, at 18:21:54
Posted by Phillipa on June 15, 2007, at 21:32:11
In reply to Re: Ie this drug may be withdrawn ? (nm), posted by linkadge on June 15, 2007, at 18:30:37
Link check your e-mails Love Jan/Phillipa
Posted by Jedi on June 15, 2007, at 23:42:56
In reply to The end of Trazodone?, posted by linkadge on June 15, 2007, at 18:21:54
> As many of you may know I have been obsessed to death with the possability that SSRI and related medicinces may cause the same type of heart dammage that fenfluramine and the recently withdrawn dopamine agonists with 5-ht2b agonism.
>
> Apparently a metabolite of trazodone, mcpp is a potent 5-ht2b agonist. I think this med may be related to similar problems.
>
> The following is a link to an article that I need to read, as it directly relates to my concerns, but I do not have the required membership.
>
> http://www.blackwell-synergy.com/doi/abs/10.1111/j.1601-5215.2007.00195.x
>
> Does anyone have Larry Hoover's email adress? You can babblemail it to me, he won't mind as he has given it to me before.
>
>
>
> LinkadgeSorry Link-Found no info on the net, but I won't restart Traz for now.
Thanks,
Jedi
Posted by Jedi on June 15, 2007, at 23:58:40
In reply to Re: The end of Trazodone? » linkadge, posted by Jedi on June 15, 2007, at 23:42:56
This study suggests 2A not 2B.
JediCARDIOVASCULAR
The 5-Hydroxytryptamine2A Receptor Is Involved in (+)-Norfenfluramine-Induced Arterial Contraction and Blood Pressure Increase in Deoxycorticosterone Acetate-Salt Hypertension
Wei Ni, Gregory D. Fink, and Stephanie W. Watts
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan
The highly effective anorexigen (+)-fenfluramine was widely used to control body weight until the association with primary pulmonary hypertension and valvular heart disease. (+)-Norfenfluramine is the major hepatic metabolite of (+)-fenfluramine and is primarily responsible for the anorexic effect as well as side effects. We reported that (+)-norfenfluramine causes vasoconstriction and a blood pressure increase in rats with normal blood pressure via the 5-hydroxytryptamine (5-HT)2A receptor. With the knowledge that (+)-norfenfluramine also has affinity for 5-HT2B receptors and that arterial 5-HT2B receptor expression is up-regulated in deoxycorticosterone acetate (DOCA)-salt hypertension, we tested the hypothesis that (+)-norfenfluramine-induced vasoconstriction and pressor effects are potentiated in DOCA-salt hypertensive rats in a 5-HT2 receptor-dependent manner. Contractions of arteries were measured using an isolated tissue bath system or myograph. Mean arterial blood pressure was measured in chronically instrumented conscious rats. Effects of (+)-norfenfluramine in stimulating arterial contraction (leftward shift versus SHAM, aorta, 5.13-fold; renal artery, 1.95-fold; mesenteric resistance artery, 1.77-fold) and raising blood pressure were significantly enhanced in hypertension. In arteries from both normotensive and hypertensive rats, (+)-norfenfluramine-induced contraction in aorta was inhibited by 5-HT2A receptor antagonists, ketanserin and LY53857 (4-isopropyl-7-methyl-9-(2-hydroxy-1-meth ylpropoxycarbonyl)4,6,6a,7,8,9,10,10a-octahydroindolo[4,3-fg]quinoline), but not by the 5-HT2B receptor antagonist, LY272015 [6-chloro-5-methyl-N-(5-quinolinyl)-2,3-dihydro-1H-indole-1-carboxamide]. Ketanserin (3 mg/kg) reduced (+)-norfenfluramine-induced pressor response in both SHAM and DOCA rats. Our results demonstrate that (+)-norfenfluramine-induced arterial contraction and blood pressure increases are potentiated in DOCA-salt hypertensive rats. However, it is the 5-HT2A receptor and not the 5-HT2B receptor that participates in these effects.--------------------------------------------------------------------------------
Received September 14, 2006; accepted February 7, 2007.
Address correspondence to: Dr. Wei Ni, B445 Life Sciences Building, Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317. E-mail: niwei@msu.edu
Posted by linkadge on June 16, 2007, at 8:36:50
In reply to Re: The end of Trazodone?, posted by Jedi on June 15, 2007, at 23:58:40
But thats just the blood pressure effect. The effect of valve regurgitation, Ie proliferation of cardiac valve tissue that dammages the valves is a separate issue that may be mediated by 5-ht2b.
The withdrawn dopamine agonists, for instance, were potent 5-ht2b agonists, but not 5-ht2a agonists, yet they had the same effect on heart valves as fenfluramine.
Linkadge
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