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Chemoreceptor
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==Physiology== * [[carotid body|Carotid bodies]] and [[Aortic body|aortic bodies]] detect changes primarily in pCO<sub>2</sub> and H<sup>+</sup> ion concentration. They also sense decrease in partial pressure of O<sub>2</sub>, but to a lesser degree than for pCO<sub>2</sub> and H<sup>+</sup> ion concentration. * The [[chemoreceptor trigger zone]] is an area of the [[medulla oblongata|medulla]] in the brain that receives inputs from [[blood]]-borne [[drug]]s or [[hormone]]s, and communicates with the [[vomiting center]] (area postrema) to induce [[vomiting]].{{Citation needed|date=July 2010}} * Primary cilia play important roles in chemosensation. In adult tissues, these cilia regulate cell proliferation in response to external stimuli, such as tissue damage. In humans, improper functioning of primary cilia is associated with important diseases known as [[Ciliopathy|ciliopathies]].<ref name="Satir2008" /> ===Control of breathing=== Particular chemoreceptors, called [[acid-sensing ion channel|ASICs]], detect the levels of [[carbon dioxide]] in the blood. To do this, they monitor the concentration of [[hydrogen ion]]s in the blood, which decrease the [[pH]] of the blood. This can be a direct consequence of an increase in carbon dioxide concentration, because aqueous carbon dioxide in the presence of [[carbonic anhydrase]] reacts to form a [[proton]] and a [[bicarbonate]] ion.{{citation needed|date=May 2015}} The response is that the respiratory centre (in the medulla), sends [[nerve impulse|nervous impulses]] to the external [[intercostal muscles]] and the [[diaphragm (anatomy)|diaphragm]], via the [[intercostal nerve]] and the [[phrenic nerve]], respectively, to increase breathing rate and the volume of the lungs during inhalation. Chemoreceptors that regulate the depth and rhythm of breathing are broken down into two categories.{{Citation needed|date=July 2010}} * [[central chemoreceptors]] are located on the ventrolateral surface of [[medulla oblongata]] and detect changes in pH of cerebrospinal fluid. They have also been shown experimentally to respond to hypercapnic hypoxia (elevated {{CO2}}, decreased O2), and eventually desensitize, partly due to redistribution of bicarbonate out of the cerebrospinal fluid (CSF) and increased renal excretion of bicarbonate.<ref>{{cite book |doi=10.1016/B978-1-4377-1679-5.00025-9 |chapter=Pulmonary Physiology |title=Pharmacology and Physiology for Anesthesia |year=2013 |last1=Lumb |first1=Andrew B. |last2=Horner |first2=Deborah |pages=445β457 |isbn=9781437716795 }}</ref> These are sensitive to pH and {{CO2}}.<ref>{{Cite web|title=Central Chemoreceptors|url=http://pathwaymedicine.org/central-chemoreceptors|access-date=2021-03-16|website=pathwaymedicine.org|language=en|archive-date=2021-04-13|archive-url=https://web.archive.org/web/20210413171352/http://pathwaymedicine.org/Central-Chemoreceptors|url-status=dead}}</ref> * [[peripheral chemoreceptors]]: consists of aortic and carotid bodies. [[Aortic body]] detects changes in blood oxygen and carbon dioxide, but not pH, while [[carotid body]] detects all three. They do not desensitize. Their effect on breathing rate is less than that of the central chemoreceptors.{{citation needed|date=May 2015}} === Heart rate === The response to stimulation of chemoreceptors on the heart rate is complicated. Chemoreceptors in the heart or nearby large arteries, as well as chemoreceptors in the lungs, can affect heart rate. Activation of these peripheral chemoreceptors from sensing decreased O<sub>2</sub>, increased CO<sub>2</sub> and a decreased pH is relayed to cardiac centers by the [[vagus nerve|vagus]] and [[glossopharyngeal nerve|glossopharyngeal nerves]] to the [medulla oblongata|medulla] of the brainstem. This increases the sympathetic nervous stimulation on the heart and a corresponding increase in heart rate and [[myocardial contractility|contractility]] in most cases.<ref>{{Cite web|url=http://www.columbia.edu/~kj3/Chapter4.htm|title=Chapter 4|website=www.columbia.edu|access-date=2017-01-29}}</ref> These factors include activation of [[stretch receptors]] due to increased ventilation and the release of circulating catecholamines. However, if respiratory activity is arrested (e.g. in a patient with a high cervical spinal cord injury), then the primary cardiac reflex to transient [[hypercapnia]] and [[Hypoxia (medical)|hypoxia]] is a profound [[bradycardia]] and coronary [[vasodilation]] through vagal stimulation and systemic vasoconstriction by sympathetic stimulation.<ref>{{cite journal |last1=Berk |first1=James L. |last2=Levy |first2=Matthew N. |title=Profound Reflex Bradycardia Produced by Transient Hypoxia or Hypercapnia in Man |journal=European Surgical Research |date=1977 |volume=9 |issue=2 |pages=75β84 |doi=10.1159/000127928 |pmid=852474 }}</ref> In normal cases, if there is reflexive increase in respiratory activity in response to chemoreceptor activation, the increased sympathetic activity on the cardiovascular system would act to increase heart rate and contractility.
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