Effects of M1 and M2 receptor agonists and blockers on dog respiration
Abstract
AIM: To study the effects of M1 and M2 receptor agonists and blockers on dog respiration.
METHODS: Using thoracic respiratory transducer and RM-86 multipurpose polygraph to determine respiratory rate (RR), tidal volume (TV), and minute ventilation volume (MVV), and DH-100G blood gas analysis instrument to analyze pO2, pCO2 and pH.
RESULTS: Pilocarpine (Pil, an M1-R subtype agonist) 0.5, 1, and 2 mg.kg-1 iv caused increases in RR, MVV, and pO2, and a decrease in pCO2. The excitatory effects of Pil were antagonized by pretreatment with pirenzepine (Pir, 3 mg.kg-1, iv) and scopolamine (Sco, 2 mg.kg-1, iv). The iv injections of a novel M2-R subtype agonist, 6 beta-acetoxy nortropane (6 beta-AN) 2, 5, and 20 micrograms.kg-1 caused decreases in RR, MVV, and pO2 and an increase of pCO2. The actions of 6 beta-AN were antagonized by iv pretreatment with AF-DX116 ¿11-2 [[2-[(diethylamino)methyl]-1-piperidinyl] acetyl]-5, 11-dihydro-6H[2,3-b][1,4]benzodiazepine-6-one, 0.5 mg.kg-1¿ and atropine (Atr, 2 mg.kg-1). Similar results were obtained when smaller doses of Pil (0.2, 0.4, and 0.8 mg.kg-1) and 6 beta-AN (0.25, 0.5, and 1 microgram.kg-1) were injected into the vertebral artery. Pir and Sco also antagonized the excitatory effects of Pil, and AF-DX116 and Atr antagonized the inhibitory effects of 6 beta-AN on respiration.
CONCLUSION: Stimulating M1-R of the respiratory center caused excitation of the respiration while stimulating the M2-R subtype caused inhibition of the respiration.
Keywords:
METHODS: Using thoracic respiratory transducer and RM-86 multipurpose polygraph to determine respiratory rate (RR), tidal volume (TV), and minute ventilation volume (MVV), and DH-100G blood gas analysis instrument to analyze pO2, pCO2 and pH.
RESULTS: Pilocarpine (Pil, an M1-R subtype agonist) 0.5, 1, and 2 mg.kg-1 iv caused increases in RR, MVV, and pO2, and a decrease in pCO2. The excitatory effects of Pil were antagonized by pretreatment with pirenzepine (Pir, 3 mg.kg-1, iv) and scopolamine (Sco, 2 mg.kg-1, iv). The iv injections of a novel M2-R subtype agonist, 6 beta-acetoxy nortropane (6 beta-AN) 2, 5, and 20 micrograms.kg-1 caused decreases in RR, MVV, and pO2 and an increase of pCO2. The actions of 6 beta-AN were antagonized by iv pretreatment with AF-DX116 ¿11-2 [[2-[(diethylamino)methyl]-1-piperidinyl] acetyl]-5, 11-dihydro-6H[2,3-b][1,4]benzodiazepine-6-one, 0.5 mg.kg-1¿ and atropine (Atr, 2 mg.kg-1). Similar results were obtained when smaller doses of Pil (0.2, 0.4, and 0.8 mg.kg-1) and 6 beta-AN (0.25, 0.5, and 1 microgram.kg-1) were injected into the vertebral artery. Pir and Sco also antagonized the excitatory effects of Pil, and AF-DX116 and Atr antagonized the inhibitory effects of 6 beta-AN on respiration.
CONCLUSION: Stimulating M1-R of the respiratory center caused excitation of the respiration while stimulating the M2-R subtype caused inhibition of the respiration.