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J Appl Physiol 84: 215-221, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 1, 215-221, January 1998

Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled beta -agonists

Paula Carvalho, Shane R. Johnson, and Nirmal B. Charan

Pulmonary Research Laboratory, Department of Veterans Affairs Medical Center, Boise, Idaho 83702; and Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington 98195

Carvalho, Paula, Shane R. Johnson, Nirmal B. Charan. Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled beta -agonists. J. Appl. Physiol. 84(1): 215-221, 1998.---We studied the dose-dependent effects of inhaled isoetharine HCl, a beta -adrenergic bronchodilator (2.5, 5.0, 10.0, and 20.0 mg), on bronchial blood flow (Qbr) in anesthetized sheep. Isoetharine resulted in a dose-dependent increase in Qbr. With a total dose of 17.5 mg, Qbr increased from baseline values of 22 ± 3.4 (SE) to 60 ± 16 ml/min (P < 0.001), an effect independent of changes in cardiac output and systemic arterial pressure. To further study whether synthesis of endogenous nitric oxide (NO) affects beta -agonist-induced increases in Qbr, we administered isoetharine (20 mg) by inhalation before and after the NO-synthase inhibitor Nomega -nitro-L-arginine methyl ester (L-NAME). Intravenous L-NAME (30 mg/kg) rapidly decreased Qbr by ~80% of baseline, whereas L-NAME via inhalation (10 mg/kg) resulted in a delayed and smaller (~22%) decrease. Pretreatment with L-NAME via both routes of administration attenuated bronchial arterial vasodilation after subsequent challenge with isoetharine. We conclude that isoetharine via inhalation increases Qbr in a dose-dependent manner and that beta -agonist-induced relaxation of vascular smooth muscle in the bronchial vasculature is partially mediated via synthesis of NO.

bronchial circulation; beta -adrenoreceptor agonists; nitric oxide; adenosine 3',5'-cyclic monophosphate

The Journal of Applied Physiology 84(1):215-221


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