Stress Modification of Drug Response

Rupe, Billy D.; Bousqet, William F.; Miya, Tom S.

doi:10.1126/science.141.3586.1186

Cited by 39 publications

(9 citation statements)

References 3 publications

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“…No study has examined the impact of stress on the expression of the cytochrome P450 2A6 isozyme. However, stress stimulates the activity of several cytochrome P450-dependent enzymes (Stitzel and Furner 1967) and enhances the biotransformation of other drugs metabolized by these enzymes (Rupe et al 1963;Bousquet et al 1965;Driever and Bousquet 1965;Chung and Brown 1976). Therefore, it seems reasonable to postulate that stress might decrease nicotine levels by increasing the activity of the microsomal cytochrome P450 2A6 monooxygenase.…”

Section: Introductionmentioning

confidence: 93%

Effects of stress on circulating nicotine and cotinine levels and in vitro nicotine metabolism in the rat

et al. 1998

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The effects of physical and psychological stress on circulating nicotine levels and conversion of nicotine to cotinine were examined in the rat. Animals received one of three dosages of nicotine (0, 6, and 12 mg/kg) via miniosmotic pumps. On day 14 of drug infusion, animals from each drug condition were randomly assigned to one of three stress conditions (noise, rubber ligature, or no stress). After 2.5 h of stress exposure, animals were killed and plasma nicotine and cotinine were measured in vivo and hepatic conversion of nicotine to cotinine was determined in vitro. Stress lowered blood nicotine levels. However, this difference was statistically significant only among animals receiving 12 mg/kg per day nicotine. In contrast, stress had no consistent effect on either measure of conversion of nicotine to cotinine in rats. Taken together, these results suggest that stress lowers circulating nicotine levels. However, the mechanism by which this occurs remains unclear.

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Section: Introductionmentioning

confidence: 93%

Effects of stress on circulating nicotine and cotinine levels and in vitro nicotine metabolism in the rat

et al. 1998

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“…First, REMs deprivation may cause pharmaco kinetic changes that result in the apparent increase of the sensitivity to imipramine and desipramine. In fact, stress ful manipulations have been reported to affect drug metabolism (17,18). However, this possibility seems un likely, since REMs deprivation did not change the effec tive dose of clomipramine that is metabolized by the same pathway as imipramine (19).…”

Section: Discussionmentioning

confidence: 80%

REM Sleep Deprivation Potentiates the Effects of Imipramine and Desipramine but Not That of Clomipramine in the Forced Swimming Test

Asakura

Matsumoto

Ohta

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-Effects of REM sleep (REMs) deprivation on the basal swimming activity and the tricyclic anti depressants-induced increase in swimming activity in the forced swimming test were investigated. Im mediately after a 48-hr period of REMs deprivation, the basal swimming activity in REMs-deprived mice was significantly higher than those in group-housed and socially isolated animals used as the control groups. The REMs deprivation-induced increase in the swimming activity was not changed by adrenoceptor an tagonists and it returned to the control levels 3 hr after the REMs deprivation treatment. Moreover, imipra mine and desipramine but not clomipramine further increased the swimming activity enhanced by REMs deprivation at doses that did not affect the activity in the control groups. The enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine remained unchanged even at 3 hr after the REMs deprivation treatment, and it was blocked by the a2-adrenoceptor antagonist yohimbine. These results suggest that the REMs deprivation-induced increase in basal swimming activity in the forced swim ming test is not mediated by adrenoceptor mechanisms, whereas the enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine may be mediated by the functional changes in a2 adrenoceptors in the brain. . Therefore, these similarities between the effects of REMs deprivation and those of chronic anti depressants raise the possibility that the antidepressants like effect of REMs deprivation in the forced swimming test may be mediated by the same mechanism(s) as those of antidepressant drugs, and that combination of REMs deprivation with antidepressant drug treatment may modi fy the effects of antidepressant drugs.We undertook the present study to determine whether an adrenoceptor mechanism is commonly involved in the REMs deprivation and the tricyclic antidepressant drugs induced increase in swimming activity in the forced swim ming test. Furthermore, to clarify whether REMs depriva tion modifies the effect of an antidepressant drug, we test ed the effects of REMs deprivation on the imipramine-, desipramine and clomipramine-induced increase in swim ming activity.

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“…Rats stressed by unilateral hind-Ieg ligation showed a significantly decreased response to the effects of hexobarbital, pentobarbital, and meprobamate (RUPE et al 1963). This effect could not be elicited in hypophysectomized or adrenalectomized animals or following treatment of intact rats with SKF 525-A.…”

Section: Stimulatingmentioning

confidence: 94%

Residue Reviews / Rückstands-Berichte

1967

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Stress Modification of Drug Response

Cited by 39 publications

References 3 publications

Effects of stress on circulating nicotine and cotinine levels and in vitro nicotine metabolism in the rat

Effects of stress on circulating nicotine and cotinine levels and in vitro nicotine metabolism in the rat

REM Sleep Deprivation Potentiates the Effects of Imipramine and Desipramine but Not That of Clomipramine in the Forced Swimming Test

Residue Reviews / Rückstands-Berichte

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