Reduction by atropine of phencyclidine hypertension and apneusis.
The aim of this study was to assess the possible role of a central cholinergic component phencyclidine (PCP)-induced hypertension. Sprague-Dawley rats, lightly anesthetized with urethane, exhibited a dose related pressor response following 0.1-1.0 mg/kg PCP i.v. After i.v. atropine pretreatment, the PCP dose-response curve was shifted to the right, and the magnitude of the pressor responses was reduced by about 50%. In addition, atropine reduced the incidence of apneusis, but had no effect on the bradycardia that accompanied the pressor responses. Methylatropine (i.v.) did not reduce the PCP pressor responses, nor did it prevent the apneusis induced by PCP. These results suggest that in addition to its direct pressor effects the activation of central cholinergic systems contribute significantly to the cardiovascular and respiratory toxicity induced by PCP.
D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced*; D010275:Parasympathetic Nervous System / Q000187:drug effects; D010622:Phencyclidine / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D012119:Respiration / Q000187:drug effects*
D001285:Atropine; D010622:Phencyclidine