Drugs online research references
Eur J Pharmacol. 1980 Oct 3;67(1):33-40.
Effects of alpha-adrenoceptor agonists and antagonists and of antidepressant drugs on pre- and postsynaptic alpha-adrenoceptors.
Brown J, Doxey JC, Handley S.
The effects of alpha-adrenoceptor agonists and antagonists and of antidepressant drugs were studied on pre- and postsynaptic alpha-adrenoceptors. The rat vas deferens, stimulated at low frequency (0.1 Hz) was used for presynaptic studies. The rat anococcygeus muscle was used in postsynaptic studies. In the agonist studies clonidine and guanfacine were selective for presynaptic alpha-adrenoceptors, methoxamine and phenylephrine were selective for postsynaptic alpha-adrenoceptors and noradrenaline and alpha-methylnoradrenaline were equipotent at pre- and post-synaptic alpha-adrenoceptors. In the antagonist studies piperoxane and yohimbine were selective for presynaptic alpha-adrenoceptors, phentolamine was equipotent at pre- and postsynaptic alpha-adrenoceptors and prazosin was a selective postsynaptic alpha-adrenoceptor antagonist. In the series of antidepressants studied, mianserin was the most potent antagonist at presynaptic alpha-adrenoceptors, followed by trazodone, amitriptyline and nortriptyline in descending order of potency. Mianserin was approximately two hundred times less potent than piperoxane as a presynaptic alpha-adrenoceptor antagonist. Viloxazine and desipramine were inactive. With the exception of viloxazine all of the antidepressants examined possessed postsynaptic alpha-adrenoceptor antagonist properties.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6106552&dopt=Abstract
Psychiatry Res. 1986 Dec;19(4):257-66.
3H-imipramine binding in depressed elderly: relationship to family history and clinical response.
Schneider LS, Fredrickson ER, Severson JA, Sloane RB.
Platelet 3H-imipramine binding (Bmax) was determined in 34 elderly (mean age 64.8) unipolar depressed outpatients who were being treated with either nortriptyline or interpersonal psychotherapy for 10 to 16 weeks, and in nondepressed elderly controls. Bmax values were decreased in the depressed group. In addition, Bmax values were depressed further in subjects with a history of depression in first degree relatives. Good clinical response with either nortriptyline or psychotherapy was associated with lower Bmax compared to those subjects who had a poorer response to treatment. Treatment nonresponders and those with a negative family history of depression had Bmax values that were somewhat decreased but not significantly different from controls. This study extends to the elderly the potential applicability of platelet 3H-imipramine binding as a marker of depressive illness, and proposes a predictor for treatment response in elderly unipolar depressed patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3809324&dopt=Abstract
Br J Pharmacol. 1986 Dec;89(4):673-83.
Activation and desensitization of presynaptic alpha 2-adrenoceptors after inhibition of neuronal uptake by antidepressant drugs in the rat vas deferens.
Garcia-Sevilla JA, Zubieta JK.
The isolated field-stimulated vas deferens of the rat (0.1 Hz, 3 ms, 30-40 V) was used to study the relationship between the in vivo inhibition of neuronal uptake of noradrenaline (NA) by cyclic antidepressant drugs and the subsequent activation/desensitization of presynaptic alpha 2-adrenoceptors. Receptor activation was indirectly measured by quantifying the ability of each drug to inhibit basal twitch responses after their acute administration. Receptor desensitization was also indirectly measured by quantifying the ability of the drugs to reduce the inhibitory effects of selective alpha 2-adrenoceptor agonists on the electrically-induced twitch responses after their long-term administration. The acute in vivo administration of desipramine and other antidepressants (0.5-10 mg kg-1; i.p.; 2 h) resulted in dose-dependent inhibitions of the basal twitch responses which were rapidly reversed to control values by idazoxan (10-5 M). In vitro, desipramine and other antidepressants also inhibited in a concentration-dependent manner (10(-9)-10(-5) M) the twitch responses. In rats pretreated 12 h earlier with reserpine (1 mg kg-1; i.p.) or oxypertine (4 mg kg-1; i.p.), desipramine (10 mg kg-1; 2 h) did not induce inhibition of the basal twitch responses or it induced a smaller effect, respectively. For the various antidepressants the degree of inhibition of the basal twitch responses (desipramine greater than protriptyline greater than nortriptyline greater than maprotiline = imipramine greater than amitriptyline greater than viloxazine greater than iprindole much greater than zimelidine) was highly correlated (r = 0.914) with the potency for blockade of [3H]-NA uptake into rat brain synaptosomes. Clonidine and xylazine inhibited in a concentration-dependent manner (10(-9)-10(-6) M) the twitch responses. The long-term (7-14 days) administration of antidepressants or cocaine (10 mg kg-1, i.p.) resulted in significant decreases in sensitivity to clonidine or xylazine. Short-term (3 days) treatment with desipramine did not reduce the sensitivity to clonidine. The results indicate that the acute in vivo inhibition of NA neuronal uptake by antidepressants leads to the activation (through endogenous NA) of presynaptic inhibitory alpha 2-adrenoceptors which results in inhibition of the twitch responses. In contrast, prolonged in vivo inhibition of NA reuptake is followed by a slow desensitization process of the same receptors which results in a reduction of sensitivity to clonidine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3028549&dopt=Abstract
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