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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Cardiovascular Physiology Concepts textbook cover

Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)


Cardiovascular Physiology Concepts textbook cover

Click here for information on Normal and Abnormal Blood Pressure, a textbook 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 (about 20% of its total catecholamine release is norepinephrine). 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 (some is also taken up by extra-neuronal tissues) where it is metabolized. A small amount of norepinephrine, however, 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) that causes very high circulating levels of catecholamine – pheochromocytoma. This can lead to a hypertensive crisis.

Circulating Epinephrine Causes:

epinephrine effects on blood pressure and heart rate

The figure below shows the effects of low, medium and high plasma concentrations of epinephrine on systemic vascular resistance. At low levels, epinephrine preferentially binds to high affinity vascular β2-adrenoceptors and causes vasdilation, 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 epineprhine. 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).

epinephrine effects on systemic vascular resistance

 

Circulating Norepinephrine Causes:

norepinephrine effects on blood pressure and heart rate

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 low dose of epinephrine is administered in the presence of alpha-adrenoceptor blockade, the unopposed β2-adrenoceptor activation will cause a large hypotensive response due to systemic vasodilation despite the cardiac stimulation that occurs due to β1-adrenoceptor activation.

Revised 05/05/15



DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.