Posted by SalArmy4me on August 12, 2001, at 8:46:55
In reply to Are Tricylic side effects really worse than SSRI's, posted by Jackster on August 12, 2001, at 5:59:05
Frazer, Alan PhD. Pharmacology of Antidepressants. Journal of Clinical Psychopharmacology. 17(2S) Supplement:2S-18S, April 1997:
"Blockade of muscarinic cholinergic receptors with Tricyclics (TCAs) causes side effects that occur quite frequently-dry mouth, blurred vision, constipation, and urinary retention. Sinus tachycardia and short-term memory impairment can also be due to muscarinic cholinergic blockade. The TCAs as a group are clearly more potent at blocking these receptors than SSRIs, and they all can cause these types of side effects. Consistent with their high potency at muscarinic receptors, amitriptyline and protriptyline tend to produce anticholinergic side effects with the highest frequency... Even though the SSRI paroxetine has reasonable affinity for muscarinic receptors, it produces less marked anticholinergic effects than the TCAs. This may be because it is given in lower dosage than many TCAS and, in general, achieves lower steady-state plasma concentrations than most of the TCAs. Because of their low potency at blocking muscarinic receptors, other SSRIs and other atypical ADs such as mirtazapine, nefazodone, and venlafaxine, cause essentially no more anticholinergic side effects than placebo.
Blockade of H1 histamine receptors with TCAs causes sedation and drowsiness, and perhaps contributes to weight gain as well. H1 histamine receptor blockade can also lead to the potentiation of the effects of other central nervous system (CNS) depressants. Among the TCAs, sedation and drowsiness are commonly seen with doxepin, trimipramine, amitriptyline, and imipramine. Interestingly, the secondary amine TCAs-desipramine, nortriptyline, and protriptyline-are less sedating than the other TCAs. This may be related to the strong noradrenergic effects of such drugs, given the postulated role of central noradrenergic neurons in arousal.
Orthostatic hypotension and perhaps sedation with TCAs are associated with blockade of alpha1 adrenoceptors. The sedative effect may be a consequence of blocking the actions of NE centrally, because NE is thought to increase arousal or vigilance. Presumably because of their relative high affinity at alpha1 adrenoceptors, all TCAs can cause orthostatic hypotension. This can occur in as many as 20% of patients treated with TCAs; it is particularly a problem in elderly patients. Because the hypotension is not consistently related to dosage, it can occur anytime during treatment. Among the TCAs, postural hypotension is observed least frequently with nortriptyline..."
poster:SalArmy4me
thread:74742
URL: http://www.dr-bob.org/babble/20010809/msgs/74757.html