TCAs potentiate the sedative effects of barbiturates, tranquilizers and depressants. Alcohol may potentiate the hypotensive effects of Moxonidine. Drugs that inhibit the breakdown of endogenous opioids also potentiate the antinociceptive effects of . Systemic agmatine can potentiate opioid analgesia and prevent tolerance to chronic morphine in laboratory rodents. Alcohol may potentiate some of the CNS depressant effects of doxepin. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. It may also potentiate the CNS depressant effects of alcohol. Concomitant use of alcohol and other sedatives may potentiate this effect. Therapeutic ADAM inhibitors might potentiate anti-cancer therapy. Other immunosuppressants like cyclosporins may potentiate methotrexate's haematologic effects, hence potentially leading to toxicity. Danshen may potentiate the effects of the anticoagulation drug warfarin, possibly causing bleeding complications. Sympathomimetics may potentiate the sympathomimetic effects of dosulepin. Alcohol can potentiate orthostatic hypotension to the point of syncope. Mutations in CCK receptors in combination with mutated CCK genes potentiate this association. For aspirin and warfarin, high amounts of vitamin E may potentiate anti-blood clotting action.