Effects of adrenoceptor blockers on the cardiorespiratory response to nicotine in rats.
Three groups of anaesthetized rats, consisting of 8 rats per group, were studied. Group 1 was the control and received intravenous injection of nicotine, 50 micrograms/kg, only. Groups II and III were pretreated with propranolol, 0.5mg/kg and prazosin, 1mg/kg respectively before 50 micrograms/kg of nicotine was injected i.v. Blood pressure, heart rate, respiratory rate and amplitude of respiratory excursion were monitored continuously before and for 1 hr after the injections. Index of Pulmonary Ventilation Rate was computed as a product of amplitude of respiratory excursion and respiratory rate. The results showed that nicotine caused an initial fall in blood pressure followed by a rise. The initial fall in blood pressure was abolished by prazosin, while propranolol abolished the pressor response. Nicotine had no effect on heart rate in the three groups. Nicotine caused an increase in respiratory rate and this effect was abolished by prazosin. Nicotine also caused an initial increase in pulmonary ventilation which was due mainly to increase in respiratory rate. It was concluded that nicotine exerts most of its cardiorespiratory effect via stimulation of alpha and beta adrenoceptors.
Fasanmade
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AA
Department of Physiology, College of Medicine, University of Ibadan, Nigeria.
Oyebola
D D
DD
D000818:Animals; D004195:Disease Models, Animal; D004347:Drug Interactions; D006439:Hemodynamics / Q000187:drug effects*; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology*; D011292:Premedication; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012119:Respiration / Q000187:drug effects*
D009538:Nicotine; D011433:Propranolol; D011224:Prazosin