Vasomotor center
| Vasomotor center | |
|---|---|
| Details | |
| Part of | Medulla |
| Identifiers | |
| Acronym(s) | VMC |
| MeSH | D014666 |
| Anatomical terminology | |
The vasomotor center (VMC) is a portion of the medulla oblongata. Together with the cardiovascular center and respiratory center, it regulates blood pressure.[1] It also has a more minor role in other homeostatic processes.[citation needed] Upon increase in carbon dioxide level at central chemoreceptors, it stimulates the sympathetic system to constrict vessels. This is opposite to carbon dioxide in tissues causing vasodilatation, especially in the brain.[2] Cranial nerves IX (glossopharyngeal nerve) and X (vagus nerve) both feed into the vasomotor centre and are themselves involved in the regulation of blood pressure.
Structure
The vasomotor center is a collection of integrating neurons in the medulla oblongata of the middle brain stem. The term "vasomotor center" is not truly accurate, since this function relies not on a single brain structure ("center") but rather represents a network of interacting neurons.[3]
Afferent fibres
The vasomotor center integrates nerve impulses from many places via the solitary nucleus:[4]
- central chemoreceptors
- aortic body chemoreceptors, which send impulses via the vagus nerves
- carotid body chemoreceptors, which send impulses via the glossopharyngeal nerves
- aortic arch high-pressure baroreceptors, which send impulses via the aortic nerve[5]
- carotid sinus high-pressure baroreceptors, which send impulses via the glossopharyngeal nerves
Efferent fibres
The vasomotor center gives off sympathetic fibres through the spinal cord and sympathetic ganglia, which reach vascular smooth muscle.[6]
Function
The vasomotor center changes vascular smooth muscle tone.[1][5] This changes local and systemic blood pressure.[1]
A drop in blood pressure leads to increased sympathetic tone from the vasomotor center.[7] This acts to raise blood pressure.[7]
Clinical significance
Methyldopa acts on the vasomotor center, leading to selective stimulation of α2-adrenergic receptor.[8] Guanfacine also causes the same stimulation.[9] This reduces sympathetic tone to vascular smooth muscle.[9] This reduces heart rate and vascular resistance.[9]
Digoxin increases vagal tone from the vasomotor centre, which decreases pulse.[7]
G-series nerve agents have their most potent effect in the vasomotor center.[10] Unlike other parts of the body, where continued stimulation of acetylcholine receptors leads to recoverable paralysis, overstimulation of the vasomotor center is often causes a fatal rise in blood pressure.[11]
History
The localization of vasomotor center was determined by Filipp Ovsyannikov in 1871.[10]
See also
References
- ^ a b c Sear, John W. (January 1, 2019), Hemmings, Hugh C.; Egan, Talmage D. (eds.), "26 - Antihypertensive Drugs and Vasodilators", Pharmacology and Physiology for Anesthesia (Second Edition), Philadelphia: Elsevier, pp. 535–555, doi:10.1016/b978-0-323-48110-6.00026-0, ISBN 978-0-323-48110-6, S2CID 220688413, retrieved November 29, 2020
- ^ "Bionic blood pressure device being developed at Vanderbilt". Retrieved October 6, 2008.
- ^ Guyenet, Patrice G. (May 2006). "The sympathetic control of blood pressure". Nature Reviews. Neuroscience. 7 (5): 335–346. doi:10.1038/nrn1902. ISSN 1471-003X. PMID 16760914. S2CID 8752032.
- ^ Northcott, Carrie A.; Haywood, Joseph R. (January 1, 2007), Lip, Gregory Y. H.; Hall, John E. (eds.), "Chapter 25 - Central Nervous System Control of Blood Pressure", Comprehensive Hypertension, Philadelphia: Mosby, pp. 281–290, doi:10.1016/b978-0-323-03961-1.50028-3, ISBN 978-0-323-03961-1
- ^ a b Schwarzwald, Colin C.; Bonagura, John D.; Muir, William W. (January 1, 2009), Muir, William W.; Hubbell, John A. E. (eds.), "Chapter 3 - The Cardiovascular System", Equine Anesthesia (Second Edition), Saint Louis: W.B. Saunders, pp. 37–100, doi:10.1016/b978-1-4160-2326-5.00003-1, ISBN 978-1-4160-2326-5, retrieved November 29, 2020
- ^ Touyz, Rhian M. (January 1, 2014), Willis, Monte S.; Homeister, Jonathon W.; Stone, James R. (eds.), "Chapter 14 - Blood Pressure Regulation and Pathology", Cellular and Molecular Pathobiology of Cardiovascular Disease, San Diego: Academic Press, pp. 257–275, doi:10.1016/b978-0-12-405206-2.00014-4, ISBN 978-0-12-405206-2, retrieved November 29, 2020
- ^ a b c Waller, Derek G.; Sampson, Anthony P. (January 1, 2018), Waller, Derek G.; Sampson, Anthony P. (eds.), "7 - Heart failure", Medical Pharmacology and Therapeutics (Fifth Edition), Elsevier, pp. 131–142, doi:10.1016/b978-0-7020-7167-6.00007-5, ISBN 978-0-7020-7167-6, retrieved November 29, 2020
- ^ O'Shaughnessy, Kevin M. (January 1, 2012), Bennett, Peter N.; Brown, Morris J.; Sharma, Pankaj (eds.), "Chapter 24 - Arterial hypertension, angina pectoris, myocardial infarction and heart failure", Clinical Pharmacology (Eleventh Edition), Oxford: Churchill Livingstone, pp. 393–427, doi:10.1016/b978-0-7020-4084-9.00063-x, ISBN 978-0-7020-4084-9, retrieved November 29, 2020
- ^ a b c Rizzo, Renata; Gulisano, Mariangela (January 1, 2013), Martino, Davide; Cavanna, Andrea E. (eds.), "Chapter Fourteen - Clinical Pharmacology of Comorbid Attention Deficit Hyperactivity Disorder in Tourette Syndrome", International Review of Neurobiology, Advances in the Neurochemistry and Neuropharmacology of Tourette Syndrome, 112, Academic Press: 415–444, doi:10.1016/b978-0-12-411546-0.00014-7, PMID 24295629, retrieved November 29, 2020
- ^ a b Owsjannikow, PH. Die tonischen und reflektorischen Centren der Gefäßnerven. / Berichte ueber die Verhandlungen der Königlich Sächsischen Gesellschaft der Wissenschaften zu Leipzig (1871) 23.
- ^ Abdollahi, M.; Mostafalou, S. (January 1, 2014), "G-Series Nerve Agents", in Wexler, Philip (ed.), Encyclopedia of Toxicology (Third Edition), Oxford: Academic Press, pp. 800–805, ISBN 978-0-12-386455-0, retrieved November 29, 2020