Portion of the medulla oblongata
Thevasomotor center (VMC ) is a portion of themedulla oblongata . Together with thecardiovascular center andrespiratory center , it regulatesblood pressure .[ 1] It also has a more minor role in otherhomeostatic processes.[citation needed ] Upon increase incarbon dioxide level atcentral 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.
The vasomotor center is a collection of integratingneurons in themedulla oblongata of the middlebrain 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]
The vasomotor center integrates nerve impulses from many places via thesolitary nucleus :[ 4]
The vasomotor center gives off sympathetic fibres through thespinal cord andsympathetic ganglia , which reach vascular smooth muscle.[ 6]
The vasomotor center changesvascular smooth muscle tone .[ 1] [ 5] This changes local and systemicblood 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 [ edit ] Methyldopa acts on the vasomotor center, leading to selective stimulation ofα2 -adrenergic receptor .[ 8] Guanfacine also causes the same stimulation.[ 9] This reducessympathetic tone to vascular smooth muscle.[ 9] This reducesheart rate andvascular resistance .[ 9]
Digoxin increasesvagal tone from the vasomotor centre, which decreasespulse .[ 7]
G-seriesnerve agents have their most potent effect in the vasomotor center.[ 10] Unlike other parts of the body, where continued stimulation ofacetylcholine receptors leads to recoverableparalysis , overstimulation of the vasomotor center is often causes a fatal rise in blood pressure.[ 11]
The localization of vasomotor center was determined byFilipp Ovsyannikov in 1871.[ 10]
^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 , retrievedNovember 29, 2020 ^ "Bionic blood pressure device being developed at Vanderbilt" . RetrievedOctober 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 , retrievedNovember 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 , retrievedNovember 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 , retrievedNovember 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 , retrievedNovember 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 , retrievedNovember 29, 2020 ^a b Owsjannikow, PH. Die tonischen und reflektorischen Centren der Gefäßnerven. / Berichte ueber die Verhandlungen derKöniglich 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 , retrievedNovember 29, 2020