Psycho-Babble Medication Thread 763432

Shown: posts 1 to 6 of 6. This is the beginning of the thread.

 

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that SSRI and related medicinces may cause the same type of heart dammage that fenfluramine and the recently withdrawn dopamine agonists with 5-ht2b agonism.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.

Linkadge

 

Re: Ie this drug may be withdrawn ? (nm)

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

 

Re: Ie this drug may be withdrawn ? » linkadge

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In reply to Re: Ie this drug may be withdrawn ?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

 

Re: The end of Trazodone? » linkadge

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that SSRI and related medicinces may cause the same type of heart dammage that fenfluramine and the recently withdrawn dopamine agonists with 5-ht2b agonism.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.
>
>
>
> Linkadge

Sorry Link-Found no info on the net, but I won't restart Traz for now.
Thanks,
Jedi

 

Re: The end of Trazodone?

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.
Jedi

CARDIOVASCULAR

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

 

Re: The end of Trazodone? » Jedi

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


This is the end of the thread.


Show another thread

URL of post in thread:


Psycho-Babble Medication | Extras | FAQ


[dr. bob] Dr. Bob is Robert Hsiung, MD, bob@dr-bob.org

Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.