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Feedforward sympathetic coronary vasodilation in exercising dogs.
M W Gorman1, J D Tune, K N Richmond
1Department of Physiology and Biophysics,University of Washington School of Medicine, Seattle, Washington 98195-7290, USA. mgorman@u.washington.edu
Journal of Applied Physiology (Bethesda, Md. : 1985)
|October 29, 2000
Summary
Sympathetic nervous system activation of beta-adrenoceptors significantly increases coronary blood flow during exercise in dogs. This feedforward vasodilation, mediated by beta-receptors, is crucial for matching oxygen supply to demand.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Autonomic Nervous System
Background:
- Exercise increases myocardial oxygen demand, necessitating a corresponding increase in coronary blood flow.
- The precise mechanisms of exercise-induced coronary vasodilation, particularly the role of sympathetic beta-adrenoceptors, are not fully elucidated.
Purpose of the Study:
- To test the hypothesis that sympathetic activation of coronary smooth muscle beta-adrenoceptors mediates exercise-induced coronary vasodilation.
- To investigate the contribution of beta-adrenoceptor-mediated vasodilation to the matching of coronary blood flow and myocardial oxygen consumption during exercise.
Main Methods:
- Ten dogs were instrumented with flow transducers and catheters to measure coronary artery blood flow and blood gases.
- Measurements were taken during treadmill exercise under conditions of control, alpha-adrenoceptor blockade (phentolamine), and combined alpha + beta-adrenoceptor blockade (phentolamine + propranolol).
- Coronary venous oxygen tension and myocardial interstitial adenosine concentrations were assessed.
Main Results:
- Exercise resulted in decreased coronary venous oxygen tension, indicating an imperfect match between blood flow and oxygen consumption.
- Alpha-adrenoceptor blockade improved this match, while combined blockade worsened it compared to control.
- Significant feedforward beta-adrenoceptor-mediated coronary vasodilation was observed during exercise.
- Adenosine concentrations did not increase during exercise, suggesting it does not compensate for the loss of beta-receptor vasodilation.
Conclusions:
- Sympathetic beta-adrenoceptor activation plays a significant role in feedforward coronary vasodilation during exercise in dogs.
- This beta-receptor-mediated vasodilation is crucial for optimizing myocardial oxygen supply-demand matching.
- Adenosine does not appear to compensate for the absence of beta-receptor-mediated vasodilation during exercise.
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