Drugs online research references
Proc Natl Acad Sci U S A. 1981 Aug;78(8):5240-4.
Differentiation of the open and closed states of the ionic channels of nicotinic acetylcholine receptors by tricyclic antidepressants.
Schofield GG, Witkop B, Warnick JE, Albuquerque EX.
The actions of two clinically important dibenzocycloheptane antidepressant drugs, amitriptyline and nortriptyline, were studied on ionic channels of nicotinic acetylcholine (AcCho) receptors at the neuromuscular junction of frog skeletal muscle. Amitriptyline (5-10 microM) and nortriptyline (1-2 microM), like imipramine (5-10 microM), did not react with the nicotinic AcCho receptor but caused a voltage- and time-dependent decrease in the peak amplitude of the endplate current (epc). The time constant of epc decay, however, retained its voltage sensitivity. The voltage- and time-dependent effect of amitriptyline was nonlinear with regard to the current/voltage (I/V) relationship. Nortriptyline also had a more pronounced voltage- and time-dependent effect evidenced by a hysteresis loop in the I/V relationship of the epc was eliminated by the use of 50-msec stepwise changes of the membrane potential. The nonlinearity and hysteresis were due to a time-dependent phenomenon and did not involve previous AcCho receptor activation. The rate constant of the voltage- and time-dependent decrease in epc amplitude was sensitive to the membrane electric field and varied linearly with the membrane potential. Iontophoretically elicited epcs were much more depressed by both drugs than were spontaneous miniature epcs. There was no effect on the time constant of miniature epc decay, single-channel lifetime, or conductance. Thus (as we have pointed out in our histrionicotoxin studies) the primary site of action of these agents presumably is the activated but nonconducting species of the ionic channel of the nicotinic AcCho receptor. These agents, particularly nortriptyline, point to several different binding sites of the ionic channel and are suitable tools for the separation of the effects on peak current amplitude from its time constant of decay.
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Int J Psychiatry Med. 1983-84;13(3):215-20.
Nortriptyline plasma levels and clinical response in patients with familial pure unipolar depression and blunted TRH tests.
Gold MS, Pottash AL, Stoll A, Martin DM, Finn LB, Extein I.
We studied the efficacy of nortriptyline (NT) when given in doses which produce tricyclic antidepressant (TCA) levels within the proposed therapeutic "window" in a select patient group to assess the "window" hypothesis in a group of patients that was biologically homogeneous with respect to the TRH test and clinically homogeneous with respect to RDC, DSM III, and Winokur criteria. Pharmacokinetic and dose differences were controlled for by administering a NT dose-prediction test, giving the indicated dose, allowing levels to reach steady state and changing the dose, if necessary, to maintain NT levels within the range of 90-130 ng/ml. Using this protocol nine of ten patients responded to NT. This rate of response for a severely depressed patient group is comparable to response data for ECT and recent European data using regular NT levels to change doses of NT and assess appropriate NT trial duration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6418677&dopt=Abstract
J Toxicol Environ Health. 1984;14(2-3):137-43.
Cardiotoxicity of tricyclic antidepressants in primary cultures of rat myocardial cells.
Acosta D, Ramos K.
Primary cultures of myocardial cells were used to evaluate the cardiotoxic potential of various tricyclic antidepressants (TCAs). Lactate dehydrogenase (LDH) leakage, cellular viability, and beating rates were measured to compare the cardiotoxicity of amitriptyline, desipramine, imipramine, and nortriptyline. Tricyclic antidepressants were added to the cultures to give final concentrations of 1 X 10(-5), 1 X 10(-4), and 1 X 10(-3) M. Treatments lasted 1 and 4 h. All TCAs tested caused significant release of LDH and decreased cellular viability when added at 1 X 10(-3) M for 1 and 4 h. Amitriptyline was the only compound that caused significant LDH release 4 h after exposure to lower doses. Decreased viability was observed 4 h after exposure to all TCAs at a concentration of 1 X 10(-4) and 1 X 10(-3) M. Arrhythmias were observed 1 h after exposure to 1 X 10(-5) and 1 X 10(-4) M amitriptyline. All doses of amitriptyline inhibited beating 4 h after exposure. Imipramine, desipramine, and nortriptyline at a concentration of 1 X 10(-5) M decreased the beating rates of cultured myocytes 1 and 4 h after exposure. Arrhythmias and/or total inhibition of beating were observed when the cultures were exposed to higher concentrations of these compounds. Based on these data, the rank order of cardiotoxicity was amitriptyline greater than imipramine = desipramine greater than nortriptyline.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6502730&dopt=Abstract
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