Regulation of large coronary arteries by beta-adrenergic mechanisms in the conscious dog.
- 1 July 1982
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 51 (1) , 56-66
- https://doi.org/10.1161/01.res.51.1.56
Abstract
We examined, in conscious dogs, the effects of beta-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 microgram/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 microgram/kg) induced changes that were qualitatively similar to those induced by isoproterenol. Prenalterol (20 micrograms/kg), a cardioselective beta 1-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 O2 content and decreased A-VO2 difference. After beta 1-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 beta-adrenergic mechanisms. Surprisingly, a major fraction of large coronary arterial dilation appeared to be either directly or indirectly due to beta 1-adrenergic receptor mechanisms, although beta 2-adrenergic effects were also significant.This publication has 18 references indexed in Scilit:
- The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholineNature, 1980
- Prenalterol, a non-selective β-adrenoceptor ligand with absolute β1-selective partial agonist activityJournal of Pharmacy and Pharmacology, 1980
- Alpha Adrenergic Vasoconstriction and Nitroglycerin Vasodilation of Large Coronary Arteries in the Conscious DogJournal of Clinical Investigation, 1980
- A comparison of the actions of ICI66082 and propranolol on cardiac and peripheral β-adrenoceptorsEuropean Journal of Pharmacology, 1975
- Characterization of the coronary vascular β‐adrenoceptor in the pigBritish Journal of Pharmacology, 1972
- Differences in Direct Effects of Adrenergic Stimuli on Coronary, Cutaneous, and Muscular VesselsJournal of Clinical Investigation, 1972
- Responses of coronary vessels to adrenergic stimuliJournal of Clinical Investigation, 1971
- Cardio‐selective β‐adrenoceptor blockade and the coronary circulationBritish Journal of Pharmacology, 1970
- Effects of a cardio-selective beta-adrenergic blocking agent on the heart and coronary circulationCardiovascular Research, 1970
- Cholinergic mechanisms on the heart and coronary circulationBritish Journal of Pharmacology, 1970