The coronary vascular response to norepinephrine (NE) in conscious dogs is biphasic: a functional hyperemia followed by an α-receptor mediated vasoconstriction. This study examined the role of nitric oxide (NO) in mediating the dilatory response to NE. Four dogs were chronically instrumented to measure left ventricular systolic and diastolic pressures (LVSP, LVEDP), maximal rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (MAP), and circumflex flow velocity (CFV). Resting control values were: LVSP 118 ±1.5 (SEM) mmHg, LVEDP 6±1.5 mmHg, dP/dtmax 2550±428 mmHg/sec, MAP 83±6 mmHg, HR 80±5 bpm, and CFV 3.4±1.4 kHz. Intracoronary (i.e.) injection of 03 μg NE caused a 53±17% increase in CFV followed by a 15±4% decrease. After blockade of NO synthesis using Nω-nitro-L-arginine (E-NA. 75 mg, i.e.), resting hemodynamic values were unchanged, but the coronary dilatory response to 20 μg acetylcholine, i.c., was reduced by 58±4%. After NO blockade the coronary flow increased only 28±11% in response to NE. The vasoconstriction was unchanged. These data indicate that the coronary response to NE in the conscious dog involves both endothelium independent and dependent components.
|State||Published - 1 Dec 1997|