Effects of vasopressors on contractile and phosphatidylinositol responses of rat trachea.

Abstract

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). 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. 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. 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.