Difference between revisions of "CORONARY ARTERIES-NEURAL FACTORS"

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==Reference(s)==
==Reference(s)==
Barrett, K.E., Barman, S.M., Boitano, S., Brooks, H.L., Weitz, M., Brian Patrick Kearns, Ganong, W.F. and Mcgraw-Hill Education (Firm (2016). Ganong’s review of medical physiology. 25th ed. New York: Mcgraw Hill Education.
Barrett, K.E., Barman, S.M., Brooks, H.L., X, J. and Ganong, W.F. (2019). Ganong’s review of medical physiology. 26th ed. New York: Mcgraw-Hill Education  
<br/>Hall, J.E. and Hall, M.E. (2020). Guyton And Hall Textbook Of Medical Physiology. 14th ed. S.L.: Elsevier - Health Science.
<br/>West, J.B. and Luks, A.M. (2021). West’s Pulmonary Pathophysiology. Lippincott Williams & Wilkins.


[[Category:Coronary Arteries]]
[[Category:Coronary Arteries]]
[[Category:Physiology]]
[[Category:Physiology]]

Latest revision as of 02:30, 21 March 2023

SUMMARY

1. Two receptors on coronary arterioles: alpha-adrenergic mediate vasoconstriction, beta-adrenergic mediate vasodilation.

2. Direct effect of noradrenaline (NA) is vasoconstriction. However, when given with a beta-blocker (blocks the inotropic & chronotropic effects), NA causes vasoconstriction.

3. This is due to the chronotropic effect (increased HR), inotropic effect (increased CO & SBP). These effects, due to coronary autoregulation, lead to vasodilation.

4. Thus the direct effect of NA on the heart is vasoconstriction but indirectly causes vasodilatation.

5. Stimulation of vagal fibers to the heart dilates the coronaries.


Reference(s)

Barrett, K.E., Barman, S.M., Brooks, H.L., X, J. and Ganong, W.F. (2019). Ganong’s review of medical physiology. 26th ed. New York: Mcgraw-Hill Education