NITRIC-OXIDE AND BETA-ADRENERGIC AGONIST-INDUCED BRONCHIAL ARTERIAL VASODILATION

In anesthetized sheep, we measured bronchial blood flow (Qbr) by an ul trasonic flow probe to investigate the interaction between inhaled nit ric oxide (NO; 100 parts/million) given for 5 min and 5 mi of aerosoli zed isoetharine (1.49 x 10(-2) M concentration). NO and isoetharine in creased Qbr 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 i soetharine further increased Qbr to 57.3 +/- 15.1 ml/min. NO synthase inhibitor N-omega-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, in 20 mi saline given iv) decreased Qbr to 14.6 +/- 2.6 ml/ min. NO given three times alternately with isoetharine progressively i ncreased Qbr from 14.6 +/- 2.6 to 74.3 +/- 17.0 ml/min, suggesting tha t NO and isoetharine potentiate vasodilator effects of each other. in three other sheep, after L-NAME, three sequential doses of isoetharine increased Qbr 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 isoetharin e are predominantly mediated through synthesis of NO. When this was fo llowed by three sequential administrations of NO, Qbr increased by 146 , 172, and 185%, respectively. Thus in the bronchial circulation there seems to be a close interaction between adenosine 3',5'-cyclic monoph osphate- and guanosine 3',5'-cyclic monophosphate-mediated vasodilatat ion.