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J Appl Physiol 82: 1918-1925, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 82, No. 6, pp. 1918-1925, June 1997
PULMONARY CIRCULATION AND LUNG FLUID BALANCE

Norepinephrine-induced contraction of isolated rabbit bronchial artery: role of alpha 1- and alpha 2-adrenoceptor activation

A. O. A. Zschauer, M. W. Sielczak, D. A. S. Smith, and A. Wanner

Division of Pulmonary and Critical Care Medicine, Mount Sinai Medical Center, University of Miami School of Medicine, Miami Beach, Florida 33140

Received 4 October 1996; accepted in final form 12 February 1997.

Zschauer, A. O. A., M. W. Sielczak, D. A. S. Smith, and A. Wanner. Norepinephrine-induced contraction of isolated rabbit bronchial artery: role of alpha 1- and alpha 2-adrenoceptor activation. J. Appl. Physiol. 82(6): 1918-1925, 1997.---The contractile effect of norepinephrine (NE) on isolated rabbit bronchial artery rings (150-300 µm in diameter) and the role of alpha 1- and alpha 2-adrenoceptors (AR) on smooth muscle and endothelium were studied. In intact arteries, NE increased tension in a dose-dependent manner, and the sensitivity for NE was further increased in the absence of endothelium. In intact but not in endothelium-denuded arteries, the response to NE was increased in the presence of both indomethacin (Indo; cyclooxygenase inhibitor) and NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthase inhibitor], indicating that two endothelium-derived factors, NO and a prostanoid, modulate the NE-induced contraction. The alpha 1-AR antagonist prazosin shifted the NE dose-response curve to the right, and phenylephrine (alpha 1-AR agonist) induced a dose-dependent contraction that was potentiated by L-NAME or removal of the endothelium. The sensitivity to NE was increased slightly by the alpha 2-AR antagonists yohimbine and idazoxan, and this effect was abolished by Indo or removal of the endothelium. Similarly, contractions induced by UK-14304 (alpha 2-AR agonist) were potentiated by Indo or removal of the endothelium. These results suggest that NE-induced contraction is mediated through activation of alpha 1- and alpha 2-ARs on both smooth muscle and endothelium. Activation of the alpha 1- and alpha 2-ARs on the smooth muscle causes contraction, whereas activation of the endothelial alpha 1- and alpha 2-ARs induces relaxation through release of NO (alpha 1-ARs) and a prostanoid (alpha 2-ARs).

endothelium-derived relaxing factors; nitric oxide; prostanoid; vasoconstriction

0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society




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