A significant α1-adrenergic receptor-mediated constrictor tone exists in the coronary circulation during exercise. This study investigated whether circulating catecholamines, neuronally released catecholamines, or both are responsible for this constrictor tone. If circulating catecholamines are primarily responsible, then the increase in coronary blood flow caused by the α1-adrenergic receptor antagonist prazosin should not be substantially altered by surgical sympathectomy of the ventricles. However, if neuronally released catecholamines are primarily involved, then the increase in flow caused by α1-blockade should be abolished. Dogs were divided into two groups, those that had undergone surgical ventricular sympathectomy and a sham-operated group. Both groups were instrumented for measurement of circumflex flow velocity, and a catheter was implanted into the circumflex artery. The dogs were subjected to an exercise stress test, and prazosin (0.5 mg) was administered into the circumflex catheter. In the sham-operated dogs, α1 blockade caused a 26% increase in circumflex flow. However, in the surgical ventricular sympathectomized dogs, α1 blockade elicited only a 5% increase in circumflex flow. The increase in flow after prazosin administration in the sham-operated dogs was significantly greater than that in the sympathectomized dogs. These results suggest that the sympathetic vasoconstrictor tone noted during exercise is due primarily to neuronally released catecholamines.
|Number of pages||7|
|Journal||Coronary Artery Disease|
|State||Published - 1991|