Heart Model
Cardiovascular Physiology Concepts Richard E. Klabunde, PhD

Cardiovascular Physiology Concepts 3e textbook cover Cardiovascular Physiology Concepts, 3rd edition textbook, Published by Wolters Kluwer (2021)

CNormal and Abnormal Blood Pressure, Physiology, Pathophysiology and Treatment book cover Normal and Abnormal Blood Pressure, published by Richard E. Klabunde (2013)

Circulating Catecholamines

Circulating catecholamines, epinephrine and norepinephrine, originate from two sources. Epinephrine is released by the adrenal medulla upon activation of preganglionic sympathetic nerves innervating this tissue. This activation occurs during times of stress (e.g., exercise, heart failure, hemorrhage, emotional stress or excitement, pain). Norepinephrine is also released by the adrenal medulla (approximately 20% of its total catecholamine release is norepinephrine); however, the primary source of circulating norepinephrine is spillover from sympathetic nerves innervating blood vessels. Normally, most of the norepinephrine released by sympathetic nerves is taken back up by the nerves (a small fraction is also taken up by extra-neuronal tissues) where it is metabolized. A small amount of norepinephrine that is recycled and metabolized diffuses into the blood and circulates throughout the body. At times of high sympathetic nerve activation, the amount of norepinephrine entering the blood increases dramatically.

There is also a specific adrenal medullary disorder (chromaffin cell tumor; pheochromocytoma) that causes very high circulating levels of catecholamines. This can lead to a hypertensive crisis.epinephrine effects on blood pressure and heart rate

Circulating Epinephrine Causes:

epinephrine effects on systemic vascular resistanceThe effects of low, medium and high plasma concentrations of epinephrine on systemic vascular resistance are shown in the bar graph. At low plasma levels, epinephrine preferentially binds to high affinity vascular β2-adrenoceptors and causes vasodilation, which results in a fall in systemic vascular resistance. As the concentration of epinephrine increases, lower affinity α-adrenoceptors begin to bind epinephrine, which partially offsets the β2-adrenoceptor-mediated vasodilatory effects of epinephrine. At high circulating concentrations, more α-adrenoceptors are bound to epinephrine and the balance of vasodilatory and vasoconstrictor actions of epinephrine shifts to net vasoconstriction (increased systemic vascular resistance).norepinephrine effects on blood pressure and heart rate


Circulating Norepinephrine Causes:

Pharmacologic Blocking of the Actions of Circulating Catecholamines

Because catecholamines act on the heart and blood vessels through alpha and beta adrenoceptors, the cardiovascular actions of catecholamines can be blocked by treatment with alpha-blockers and beta-blockers. Blocking either the alpha or beta adrenoceptor alone alters the response of the catecholamine because the other adrenoceptor will still bind to the catecholamine. For example, if a moderate dose of epinephrine is administered in the presence of alpha-adrenoceptor blockade, vascular β2-adrenoceptor activation unopposed by vascular α-adrenoceptor activation will cause a large hypotensive response because of systemic vasodilation despite the cardiac stimulation that occurs through β1-adrenoceptor activation.

Revised 12/7/2022




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