By U. Tufail. New England Law. 2018.
The SSRIs have also been added to the list of effective not absolutely clear at this time purchase viagra sublingual 100 mg amex impotence and high blood pressure. In reviewing the pharmacotherapy of panic disorder purchase viagra sublingual 100 mg visa erectile dysfunction viagra does not work, den Boer (89) notes that antidepressants are more effective than benzodiazepines in reducing associ- Clinical Studies ated depressive symptomatology and are at least as effective In 1986, the FDA approved the 5-HT1A partial agonist for improving anxiety, agoraphobia, and overall impair- for generalized anxiety disorder. Bell and Nutt (90) remark that SSRIs improve 60% challenge the benzodiazepines for this patient group and to 70% of panic patients, a similar percentage to those seen was generally perceived as an improvement because of the with the TCAs. The efficacy of buspir- Like OCD, panic disorder is well treated by SSRIs but one, however, was not the same as that of the benzodiaze- does not appear to be effectively treated by receptor specific pines in terms of its delayed onset of action, and it is gener- compounds. Using the 5-HT1A receptor diazepam and alprazolam (81). The 5-HT1A partial agonist agonist flesinoxan, van Vliet et al. It has also been reported that the 5-HT2A/2C an- D2 antagonist and is extensively metabolized. One of the tagonist ritanserin had no effects on panic attacks or phobic major metabolites, 1-pyrimidinylpiperazine (1-PP), may avoidance, and a similar negative finding has been reported contribute to the pharmacologic activity of buspirone (82). In a double-blind, placebo-controlled study of buspirone in GAD patients (83), the drug was reported to be as effica- cious as lorazepam at the end of a 4-week treatment period. NEUROKININ RECEPTOR ANTAGONISTS After the drugs were discontinued, however, the lorazepam- Rationale treated patients worsened whereas the buspirone-treated subjects maintained clinical improvement. Thus, there con- There is an extensive literature demonstrating that the pep- tinues to be evidence that buspirone is effective in GAD. In addi- was discontinued, but these early clinical data will undoubt- tion, anatomic and physiologic evidence has also indicated edly lead to further clinical evaluation of NK-1 antagonists. Preclinical volved in the regulation of mood and affect, such as the studies have shown that NK-2 antagonists such as amygdala, hypothalamus, and periaqueductal gray (97). GR159897 and SR48968 have also demonstrated activity This notion is supported by early positive clinical findings in social interaction and exploration anxiolytic models, and using a selective neurokinin-1 (NK-1) antagonist for the activity has been reported in the marmoset monkey using treatment of depression and anxiety (98). Good therapeutic ratios were de- scribed for these agents. NK-3 antagonists described in the literature include os- Molecular Mechanism of Action netant (Sanofi-Synthelabo), talnetant, PD-161182, and Tachykinins collectively refer to small peptides that include PD-157672 (Parke-Davis). The latter two have been desig- substance P (SP), neurokinin A (NK-A), and neurokinin B nated for the treatment of anxiety disorders, though there (NK-B). These peptides showpreferential affinity for three have been no reports of clinical trials with any NK-3 antago- receptors, designated NK-1, NK-2, and NK-3, respectively, nist for this indication. It should be noted that preclinical which are members of the seven-transmembrane, G-pro- data described to date are sparse, and there is some sugges- tein–coupled family. Of these three receptors, NK-1 and tion that NK-3 agonism may produce an anxiolytic profile. NK-3 are found in the brain, whereas NK-2 is primarily Thus, intraventricular administration of the NK-3 agonist localized peripherally in smooth muscle of the respiratory, senktide produced anxiolytic effects in mice that could be urinary, and gastrointestinal tracts. Neurokinin receptors blocked by administration of the NK-3 antagonist SR are localized in a number of different brain areas that are 142801, and SR 142801 was found to have some anxiogenic implicated in anxiety, including the amygdala, hypothala- activity (100). Studies assessing the effects of direct administration of neurokinin agonists such as substance P into the nervous Future Drugs and Directions system are complicated by the findings that, depending on Further depression and anxiety clinical trials with centrally factors such as the site and dose, opposite effects on behavior active NK-1 antagonists are needed to provide further vali- may be achieved. In addition, further assessment of the Current Drugs in Development role of NK-2 and NK-3 subtypes is needed to determine the possible relevance, if any, of these receptor subtypes. Numerous NK-1 antagonists have been described in the literature, including MK-869 (Merck) and an analogue, L- 760,735 (Merck), SR140333 (Sanofi), CP-122,721 (Pfizer), RP67580 (Rhone-Poulenc), FK-888 (Fujisawa), GLUTAMATE RECEPTOR AGONISTS AND SDZ NKT 343 (Novartis), and PD 154075 (Parke-Davis). MODULATORS NK-1 antagonists have been reported to demonstrate anxio- Rationale lytic effects in animal models such as social interaction (99), though these effects are not consistently seen across all com- Glutamate is the major mediator of excitatory neurotrans- pounds (34). Researchers from Merck have reported that mission in the CNS. Despite this ubiquity, the elucidation vocalizations elicited by maternal separation in guinea pigs of numerous glutamate receptor subtypes with differential are robustly blocked by NK-1 antagonists such as MK-869, localizations in the brain, and the development of selective an effect that is shared by a range of antidepressant and pharmacologic agents, has led to the realization that gluta- anxiolytic agents (98).
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