PURPOSE: Vasopressors, such as dopamine (DA), norepinephrine (NE), and phenylephrine (Phe), are commonly used during anesthesia to increase blood pressure through alpha(1)-adrenoceptors. The present study was designed to examine the effects of DA, NE, and Phe on the contractile and phosphatidylinositol (PI) responses of the rat trachea induced by a muscarinic agonist, carbachol (CCh). METHODS: A rat tracheal ring was suspended between two stainless-steel hooks in Krebs-Henseleit (K-H) solution. Contraction was induced with 0.55 microM CCh, and 30 min later DA, NE, or Phe was added. The tracheal slices were incubated in K-H solution containing LiCl, (3)[H] myo-inositol, and CCh in the presence or absence of DA, NE, or Phe. The (3)[H]inositol monophosphate (IP(1)) formed was measured. RESULTS: CCh caused tracheal ring contraction. NE attenuated CCh-induced contraction at a dose of 1 microM or greater and had a maximal effect at 3 microM. DA and Phe did not affect CCh-induced contraction. CCh-induced IP(1) accumulation was potentiated significantly by NE and Phe, but not by DA. CONCLUSION: Although NE and Phe potentiated CCh-induced IP(1) accumulation, they could not potentiate CCh-induced contraction, suggesting that in clinical settings, vasopressors such as NE, DA, and Phe might be safely used in patients with asthma.
PURPOSE: Vasopressors, such as dopamine (DA), norepinephrine (NE), and phenylephrine (Phe), are commonly used during anesthesia to increase blood pressure through alpha(1)-adrenoceptors. The present study was designed to examine the effects of DA, NE, and Phe on the contractile and phosphatidylinositol (PI) responses of the rat trachea induced by a muscarinic agonist, carbachol (CCh). METHODS: A rat tracheal ring was suspended between two stainless-steel hooks in Krebs-Henseleit (K-H) solution. Contraction was induced with 0.55 microM CCh, and 30 min later DA, NE, or Phe was added. The tracheal slices were incubated in K-H solution containing LiCl, (3)[H] myo-inositol, and CCh in the presence or absence of DA, NE, or Phe. The (3)[H]inositol monophosphate (IP(1)) formed was measured. RESULTS:CCh caused tracheal ring contraction. NE attenuated CCh-induced contraction at a dose of 1 microM or greater and had a maximal effect at 3 microM. DA and Phe did not affect CCh-induced contraction. CCh-induced IP(1) accumulation was potentiated significantly by NE and Phe, but not by DA. CONCLUSION: Although NE and Phe potentiated CCh-induced IP(1) accumulation, they could not potentiate CCh-induced contraction, suggesting that in clinical settings, vasopressors such as NE, DA, and Phe might be safely used in patients with asthma.