Regulation of Large Coronary Arteries by yS-Adrenergic Mechanisms in the Conscious Dog

We examined, in conscious dogs, the effects of /?-adrenergic stimulation on measurements of left circumflex coronary arterial diameter and blood flow and on calculations of late diastolic coronary resistance (LDCR) and left circumflex coronary internal cross-sectional area (CSA). Isoproterenol (0.1 fig/kg) initially decreased mean arterial pressure by 25 ± 2% (mean ± SEM), and LDCR by 62 ± 4%, and increased heart rate by 82 ± 10%, left ventricular (LV) dP/dt by 79 ± 12%, and mean coronary blood flow by 85 ± 5%, while CSA rose slightly. The peak effects on CSA (24 ± 2%) occurred later, along with decreases in mean arterial pressure (7.4 ± 1.0%) and LDCR (25 ± 5.3%) and increases in coronary blood flow (14 ± 2%), LV dP/dt (12 ± 3%), and heart rate (24 ± 4%). Pirbuterol (1.0 jug/kg) induced changes that were qualitatively similar to those induced by isoproterenol. Prenalterol (20 /xg/kg), a cardioselective /?i-adrenergic receptor agonist, did not affect mean arterial pressure, but increased heart rate by 40 ± 5%, LV dP/dt by 72 ± 10%, mean coronary blood flow by 34 ± 11%, and CSA by 26 ± 3%, and decreased LDCR by 29 ± 5%. Isoproterenol and pirbuterol, but not prenalterol, increased coronary sinus Oj content and decreased A-V O> difference. After /?i-adrenergic receptor blockade with atenolol (1 mg/kg), prenalterol no longer induced significant effects, whereas isoproterenol and pirbuterol decreased mean arterial pressure similarly to what was observed prior to blockade, but did not increase LV dP/dt, and induced attenuated increases in mean coronary blood flow, CSA, and decreases in LDCR. Thus, in the intact, conscious animal, large coronary arteries are regulated by /J-adrenergic mechanisms. Surprisingly, a major fraction of large coronary arterial dilation appeared to be either directly or indirectly due to fi\adrenergic receptor mechanisms, although /?2-adrenergic effects were also significant. (C/rc Res 51: 56-66, 1982)