Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled beta-agonists
| Autor: | Paula Carvalho, Nirmal B. Charan, Shane R. Johnson |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Agonist
medicine.medical_specialty Physiology medicine.drug_class Hemodynamics Vasodilation Bronchial Arteries Nitric oxide chemistry.chemical_compound Phenylephrine Oxygen Consumption Physiology (medical) medicine.artery Internal medicine Administration Inhalation Cyclic AMP Isoetharine Medicine Animals Enzyme Inhibitors Sheep Dose-Response Relationship Drug business.industry Bronchial circulation Adrenergic beta-Agonists Endocrinology NG-Nitroarginine Methyl Ester chemistry Circulatory system Injections Intravenous Nitric Oxide Synthase business Bronchial artery Adrenergic alpha-Agonists medicine.drug |
| Zdroj: | Journal of applied physiology (Bethesda, Md. : 1985). 84(1) |
| ISSN: | 8750-7587 |
| Popis: | Carvalho, Paula, Shane R. Johnson, Nirmal B. Charan.Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled β-agonists. J. Appl. Physiol. 84(1): 215–221, 1998.—We studied the dose-dependent effects of inhaled isoetharine HCl, a β-adrenergic bronchodilator (2.5, 5.0, 10.0, and 20.0 mg), on bronchial blood flow (Q˙br) in anesthetized sheep. Isoetharine resulted in a dose-dependent increase in Q˙br. With a total dose of 17.5 mg, Q˙br 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 β-agonist-induced increases in Q˙br, we administered isoetharine (20 mg) by inhalation before and after the NO-synthase inhibitor N ω-nitro-l-arginine methyl ester (l-NAME). Intravenous l-NAME (30 mg/kg) rapidly decreased Q˙br 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 Q˙br in a dose-dependent manner and that β-agonist-induced relaxation of vascular smooth muscle in the bronchial vasculature is partially mediated via synthesis of NO. |
| Databáze: | OpenAIRE |
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