Charan N. B.

Nakane T.

Nirmal B. Charan

Paula Carvalho

Rebich S.

S. Lakshminarayan

Shane R. Johnson

Trivella M. G.

White S. W.

William H. Thompson

 Charan, Nirmal B., Shane R. Johnson, S. Lakshminarayan, William H. Thompson, and Paula Carvalho. Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation. J. Appl. Physiol. 82(2): 686–692, 1997.—In anesthetized sheep, we measured bronchial blood flow (Q˙br) by an ultrasonic flow probe to investigate the interaction between inhaled nitric oxide (NO; 100 parts/million) given for 5 min and 5 ml of aerosolized isoetharine (1.49 × 10−2 M concentration). NO and isoetharine increased Q˙br from 26.5 ± 6.5 to 39.1 (SE) ± 10.6 and 39.7 ± 10.7 ml/min, respectively ( n = 5). Administration of NO immediately after isoetharine further increasedQ˙br to 57.3 ± 15.1 ml/min. NO synthase inhibitor N ω-nitro-l-arginine methyl ester hydrochloride (l-NAME; 30 mg/kg, in 20 ml saline given iv) decreased Q˙br to 14.6 ± 2.6 ml/min. NO given three times alternately with isoetharine progressively increased Q˙br from 14.6 ± 2.6 to 74.3 ± 17.0 ml/min, suggesting that NO and isoetharine potentiate vasodilator effects of each other. In three other sheep, afterl-NAME, three sequential doses of isoetharine increased Q˙br from 10.2 ± 3.4 to 11.5 ± 5.7, 11.7 ± 4.7, and 13.3 ± 5.7 ml/min, respectively, indicating that effects of isoetharine are predominantly mediated through synthesis of NO. When this was followed by three sequential administrations of NO, Q˙br increased by 146, 172, and 185%, respectively. Thus in the bronchial circulation there seems to be a close interaction between adenosine 3′,5′-cyclic monophosphate- and guanosine 3′,5′-cyclic monophosphate-mediated vasodilatation. </jats:p

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Journal of Applied Physiology

Nitric oxide and β-adrenergic agonist-induced  bronchial arterial vasodilation

Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation

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