Effects of Catecholamines on the Heart

Upon commencement of high-intensity physical activity (a struggle in these cases), the adrenal glands secrete epinephrine and norepinephrine into the blood. Most of the alpha adrenergic receptors on effector organs (cardiac muscle, smooth muscle) are alpha-1 receptors. Stimulation results in smooth muscle contraction of blood vessels, with resultant vasospasm. The beta-1 receptors are primarily in the heart; the beta-2 receptors in the heart and peripherally. Stimulation of the beta-1 receptors causes an increase in heart rate, contractility and conduction velocity. Beta-2 stimulation results in smooth muscle relaxation. Epinephrine reacts with alpha and beta receptors both peripherally and in the cardiovascular system. Norepinephrine has its predominant effect on the cardiovascular system, reacting with the alpha-1 and beta-1 receptors in the effector cells of the heart. Thus, both epinephrine and norepinephrine react with beta-1 receptors with resultant increase in heart rate, contractility and conduction velocity. Coronary arteries have in their walls both beta-2 and alpha-1 receptors, with the beta-2 more plentiful. Norepinephrine interacting only with the alpha-1 receptors causes vasoconstriction, thus decreasing the amount of oxygenated blood being supplied to the myocardium by the coronary arteries. Therefore, any drug that causes increased exposure of receptor sites to norepinephrine predisposes to coronary artery constriction at the time the heart needs more — not less — oxygen. At the same time that changes in catecholamine concentrations are occurring, the aforementioned changes in blood potassium levels also occur.

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