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Since cocaine or diazepam are used clinically and/or abused concomitantly with narcotics, this study was designed to determine if morphine-dependent, morphine-withdrawn, or acute morphine rats exhibit an altered core body temperature at 24 or 4 °C to either cocaine (10, 20, or 30 mg/kg i.p.) or diazepam (2 or 4 mg/kg i.p.). At 24 °C, each dose of cocaine manifested hyperthermia in all groups of rats except morphine-dependent whereas at 4 °C cocaine produced hypothermia in all groups except morphine-dependent. At both 24 and 4°C, diazepam, 2 or 4 mg/kg, caused a hypothermic response in control, dependent, and withdrawn animals. At 24 °C, administration of acute morphine alone induced a hyperthermia which was antagonized by both doses of diazepam. At 4°C, acute morphine alone induced an initial hypothermia followed by a hyperthermia; both doses of diazepam potentiated the hypothermic response to acute morphine. Thus, significant alterations in core body temperature may be induced following the administration of cocaine or diazepam to morphine-treated rats.

Acetylcholine-induced catecholamine secretion from isolated, perfused bovine adrenal medulla was strongly inhibited by hydrocortisone (30 μM), estradiol (30 μM), and estriol (30 μM). Diethylstilbestrol (DES) (10 and 30 μM) inhibited acetylcholine-induced secretion, and the effect of the higher dose was prolonged. Inhibition of high potassium-induced secretion by DES (30 μM) indicated that hormonal inhibition of evoked secretion was not by competition for acetylcholine-sensitive receptor sites. Dihydrotestosterone (30 μM) was ineffective in inhibiting acetylcholine-induced secretion. Hydrocortisone, estradiol, and estriol treatments enhanced nonstimulated release. It is suggested that incorporation of certain steroids into plasma and granule membranes, thereby modifying membrane function, enhances nonstimulated release and may also block evoked release of secretory material.

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