Editing Homeostasis (section)

===Calcium levels===
{{main|Calcium metabolism#Regulation of calcium metabolism}}
[[File:625 Calcium Homeostasis.jpg|thumb|upright=1.4 |Calcium homeostasis]]
The plasma ionized calcium (Ca<sup>2+</sup>) concentration is very tightly controlled by a pair of homeostatic mechanisms.<ref name=Brini>{{cite book | first1 = Marisa | last1 = Brini | first2 = Denis | last2 = Ottolini | first3 = Tito | last3 = Calì | first4 = Ernesto | last4 = Carafoli | chapter = Calcium in Health and Disease | editor-first1 = Astrid | editor-last1 = Sigel  | editor-last2 = Helmut | editor-first2 = Roland K. O. | title = Interrelations between Essential Metal Ions and Human Diseases | series = Metal Ions in Life Sciences | volume = 13 | year = 2013 | publisher = Springer | pages = 81–137 | doi = 10.1007/978-94-007-7500-8_4 | pmid = 24470090 | isbn = 978-94-007-7499-5 }}</ref> The sensor for the first one is situated in the [[parathyroid glands]], where the [[Parathyroid gland#Histology|chief cells]] sense the Ca<sup>2+</sup> level by means of specialized calcium receptors in their membranes. The sensors for the second are the [[parafollicular cells]] in the [[thyroid gland]]. The parathyroid chief cells secrete [[parathyroid hormone]] (PTH) in response to a fall in the plasma ionized calcium level; the parafollicular cells of the thyroid gland secrete [[calcitonin]] in response to a rise in the plasma ionized calcium level.

The [[Effector (biology)|effector]] organs of the first homeostatic mechanism are the [[bone]]s, the [[kidney]], and, via a hormone released into the blood by the kidney in response to high PTH levels in the blood, the [[duodenum]] and [[jejunum]]. Parathyroid hormone (in high concentrations in the blood) causes [[bone resorption]], releasing calcium into the plasma. This is a very rapid action which can correct a threatening [[hypocalcemia]] within minutes. High PTH concentrations cause the excretion of [[Phosphate|phosphate ions]] via the urine. Since phosphates combine with calcium ions to form insoluble salts (see also [[bone mineral]]), a decrease in the level of phosphates in the blood, releases free calcium ions into the plasma ionized calcium pool. PTH has a second action on the kidneys. It stimulates the manufacture and release, by the kidneys, of [[calcitriol]] into the blood. This [[steroid]] hormone acts on the epithelial cells of the upper small intestine, increasing their capacity to absorb calcium from the gut contents into the blood.<ref>{{cite book |last1= Stryer |first1= Lubert | title=In: Biochemistry. |chapter= Vitamin D is derived from cholesterol by the ring-splitting action of light.|page=707 |edition=  Fourth |location= New York |publisher= W.H. Freeman and Company|date= 1995 |isbn= 0-7167-2009-4 }}</ref>

The second homeostatic mechanism, with its sensors in the thyroid gland, releases calcitonin into the blood when the blood ionized calcium rises. This hormone acts primarily on bone, causing the rapid removal of calcium from the blood and depositing it, in insoluble form, in the bones.<ref>{{Cite journal|last1=Felsenfeld|first1=A. J.|last2=Levine|first2=B. S.|date=2015-03-23|title=Calcitonin, the forgotten hormone: does it deserve to be forgotten?|url=https://dx.doi.org/10.1093/ckj/sfv011|journal=Clinical Kidney Journal|volume=8|issue=2|pages=180–187|doi=10.1093/ckj/sfv011|pmid=25815174|issn=2048-8505|pmc=4370311|access-date=18 June 2021|archive-date=6 March 2022|archive-url=https://web.archive.org/web/20220306112843/https://academic.oup.com/ckj/article/8/2/180/471044|url-status=live}}</ref>

The two homeostatic mechanisms working through PTH on the one hand, and calcitonin on the other can very rapidly correct any impending error in the plasma ionized calcium level by either removing calcium from the blood and depositing it in the skeleton, or by removing calcium from it. The [[skeleton]] acts as an extremely large calcium store (about 1&nbsp;kg) compared with the plasma calcium store (about 180&nbsp;mg). Longer term regulation occurs through calcium absorption or loss from the gut.

Another example are the most well-characterised [[Cannabinoid|endocannabinoids]] like [[anandamide]] (''N''-arachidonoylethanolamide; AEA) and [[2-Arachidonoylglycerol|2-arachidonoylglycerol]] (2-AG), whose synthesis occurs through the action of a series of [[intracellular]] [[enzyme]]s activated in response to a rise in intracellular calcium levels to introduce homeostasis and prevention of [[Neoplasm|tumor]] development through putative protective mechanisms that prevent [[cell growth]] and [[Metastasis|migration]] by activation of [[Cannabinoid receptor type 1|CB1]] and/or [[Cannabinoid receptor type 2|CB2]] and adjoining [[Cannabinoid receptor#Other cannabinoid receptors|receptors]].<ref>{{Cite journal|last1=Ayakannu|first1=Thangesweran|last2=Taylor|first2=Anthony H.|last3=Marczylo|first3=Timothy H.|last4=Willets|first4=Jonathon M.|last5=Konje|first5=Justin C.|date=2013|title=The Endocannabinoid System and Sex Steroid Hormone-Dependent Cancers|journal=International Journal of Endocrinology|volume=2013|pages=259676|doi=10.1155/2013/259676|issn=1687-8337|pmc=3863507|pmid=24369462|doi-access=free}}</ref>