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Regulation of coronary resistance vessels and large coronary arteries
Insights
Alpha-adrenergic receptors regulate coronary blood flow and large coronary arteries. Blocking these receptors or stimulating vasodilation reversed vasoconstriction, revealing key mechanisms in coronary vascular regulation.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
Background:
- Alpha-adrenergic receptors play a role in regulating coronary arteries.
- Previous studies suggest alpha-adrenergic agents can cause vasoconstriction or vasodilation.
Purpose of the Study:
- To investigate the role of alpha-adrenergic receptors in regulating coronary resistance vessels and large coronary arteries.
- To determine the effects of specific alpha-adrenergic agonists and antagonists on coronary hemodynamics.
Main Methods:
- Studies in chronically instrumented conscious animals.
- Infusion of norepinephrine, phenylephrine, and B-HT 920.
- Alpha-adrenergic blockade using prazosin and rauwolscine.
- Measurement of coronary blood flow and arterial pressure.
- Utilizing ultrasonic crystals to measure epicardial coronary artery diameter in conscious dogs.
Main Results:
- Low-dose norepinephrine caused coronary vasoconstriction, which was reversed to vasodilation by alpha-adrenergic blockade.
- Stimulation of alpha 1 and alpha 2 receptors increased coronary vascular resistance, effects abolished by selective blockade.
- Carotid chemoreceptor reflex induced coronary vasoconstriction, eliminated by alpha-adrenergic blockade or denervation/adrenalectomy.
- Methoxamine induced coronary artery constriction, while nitroglycerin and calcium-channel blockers caused vasodilation.
Conclusions:
- Alpha-adrenergic receptors significantly regulate both coronary resistance vessels and large coronary arteries.
- Selective blockade of alpha 1 and alpha 2 receptors can abolish adrenergic effects on coronary resistance.
- Large coronary arteries are responsive to alpha-adrenergic stimulation, exhibiting constriction, and also to metabolic demands.
Abstract:
There is now considerable evidence for alpha-adrenergic regulation of coronary resistance vessels and large coronary arteries based on studies of chronically instrumented, conscious animals. Infusion of norepinephrine at low doses causes reduction of coronary blood flow with a slight increase in arterial pressure, indicating intense coronary vasoconstriction. This coronary constrictor response was reversed to coronary vasodilation with infusion of norepinephrine after alpha-adrenergic blockade. Stimulation of alpha 1- and alpha 2-adrenergic receptors with phenylephrine and B-HT 920, respectively, also increased calculated coronary vascular resistance in the conscious animal. These effects were eliminated by selective alpha 1-adrenergic blockade with prazosin and by selective alpha 2-adrenergic blockade with rauwolscine. Stimulation of the carotid chemoreceptor reflex elicits a period of intense coronary vasoconstriction, characterized by a decrease in coronary blood flow despite increased arterial driving pressure. This response was eliminated by prior alpha-adrenergic blockade or a combination of cardiac sympathetic denervation and adrenalectomy. Using chronically implanted ultrasonic crystals to measure the epicardial coronary diameter instantaneously and continuously in conscious dogs, marked vasodilation of the large coronary arteries was observed with administration of nitroglycerin or calcium-channel antagonists; in contrast, activation of alpha-adrenergic receptors with methoxamine induced substantial constriction, characterized by a reduction in coronary artery diameter in the face of elevated distending pressure. The regulation of large coronary arteries is further complicated by the fact that these vessels are responsive to changes in myocardial metabolic demands and coronary blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)