Editing Collecting duct system (section)

==Structure==
===Segments===
[[File:Gray1133.png|thumbnail|Simple columnar epithelium and simple cuboidal epithelium in the collecting ducts of the [[pig]] [[kidney]]. The walls of the large and small [[connecting tubule]]s (a and b respectively), the circular structures, are formed by simple columnar epithelium (a) and simple cuboidal epithelium (b).]]
The segments of the system are as follows:

{| class="wikitable"
!Segment
!Description
|-
| ''[[connecting tubule]]'' ||Connects distal convoluted tubule to the cortical collecting duct 
|-
| ''initial collecting tubule'' || Before convergence of nephrons
|-
| ''cortical collecting ducts'' ||Receives filtrate from the initial collecting tubules, and descends into the [[renal medulla]], forming medullary collecting ducts
|-
| ''medullary collecting ducts'' ||
|-
| ''[[papillary ducts]]'' ||
|}

====Connecting tubule====
With respect to the [[renal corpuscle]], the '''connecting tubule''' ('''CNT''', or '''junctional tubule''', or '''arcuate renal tubule''') is the most proximal part of the collecting duct system. It is adjacent to the [[distal convoluted tubule]], the most distal segment of the [[renal tubule]]. Connecting tubules from several adjacent nephrons merge to form cortical collecting tubules, and these may join to form cortical collecting ducts (CCD).<ref>{{cite journal | author=Imai M | title=The connecting tubule: a functional subdivision of the rabbit distal nephron segments | journal=Kidney Int | year=1979 | pages=346–56 | volume=15 | issue=4 | pmid=513494 | doi=10.1038/ki.1979.46| doi-access=free }}</ref> Connecting tubules of some [[juxtamedullary nephron]]s may arch upward, forming an arcade. It is this "arcuate" feature which gives the tubule its alternate name.

The connecting tubule derives from the [[metanephric blastema]], but the rest of the system derives from the [[ureteric bud]].<ref>{{Cite book|last=Mitchell, B. S.|title=Embryology: an illustrated colour text|date=2009|publisher=Churchill Livingstone/Elsevier|others=Sharma, Ram, Britton, Robert.|isbn=978-0-7020-5081-7|edition=2nd|location=Edinburgh|pages=50–51|oclc=787843894}}</ref> Because of this, some sources group the connecting tubule as part of the [[nephron]], rather than grouping it with the collecting duct system.

{{anchor|Initial collecting tubule}}
The initial collecting tubule is a segment with a constitution similar as the collecting duct, but before the convergence with other tubules.

{{anchor|Cortical collecting duct}}
The "cortical collecting ducts" receive filtrate from multiple initial collecting tubules and descend into the [[renal medulla]] to form medullary collecting ducts.

It participates in the regulation of [[water]] and [[electrolyte]]s, including [[sodium]], and [[chloride]].<ref>{{cite book |author1=Eaton, Douglas C. |author2=Pooler, John P. | title=Vander's Renal Physiology | publisher=Lange Medical Books/McGraw-Hill | year=2004 | edition=6th | isbn=0-07-135728-9}}</ref> The CNT is sensitive to both [[isoprotenerol]] (more so than the cortical collecting ducts) and [[antidiuretic hormone]] (less so than the cortical collecting ducts), the latter largely determining its function in water reabsorption.

====Medullary collecting duct==== <!--Medullary collecting duct redirects here-->
"Medullary collecting ducts" are divided into outer and inner segments, the latter reaching more deeply into the medulla. The variable reabsorption of water and, depending on fluid balances and hormonal influences, the reabsorption or secretion of sodium, potassium, hydrogen and bicarbonate ion continues here. Urea passively transports out of duct here and creates 500mOsm gradient.

{{anchor|Outer segment}}<!--Outer medullary collecting duct redirects here-->
The outer segment of the medullary collecting duct follows the cortical collecting duct. It reaches the level of the renal medulla where the [[thin descending limb of loop of Henle]] borders with the [[thick ascending limb of loop of Henle]]<ref>{{Cite book|last = Boron|first=Walter F.|title=Medical Physiology: A Cellular and Molecular Approach| edition = updated| publisher=Elsevier/Saunders|location=Philadelphia |year=2005 |isbn=1-4160-2328-3}}</ref>{{rp|837}}

{{anchor|Inner segment}} <!--Inner medullary collecting duct redirects here-->
The inner segment is the part of the collecting duct system between the outer segment and the papillary ducts.

====Papillary duct====
'''Papillary (collecting) ducts''' are anatomical structures of the [[kidneys]], previously known as the '''ducts of [[Lorenzo Bellini|Bellini]]'''. Papillary ducts represent the most [[distal]] portion of the [[collecting duct]]. They receive [[Renal filtration|renal filtrate]] (precursor to [[urine]]) from several [[medullary collecting duct]]s and empty into a [[minor calyx]]. Papillary ducts continue the work of water reabsorption and electrolyte balance initiated in the [[collecting tubules]].<ref>{{Cite book|title = Junqueira's Basic Histology|last = Mescher|first = Anthony|publisher = McGraw-Hill|year = 2013|isbn = 9780071807203|pages = 385–403}}</ref>

[[Medullary collecting duct]]s converge to form a central (papillary) duct near the apex of each [[Renal pyramids|renal pyramid]]. This "papillary duct" exits the renal pyramid at the [[renal papilla]]e. The [[Renal filtration|renal filtrate]] it carries drains into a [[Renal calyx|minor calyx]] as [[urine]].<ref name=":0">{{Cite book|title = Junqueira's Basic Histology|last = Mescher|first = Anthony|publisher = McGraw-Hill|year = 2013|isbn = 9780071807203|pages = 400}}</ref>

The cells that comprise the duct itself are similar to rest of the collecting system. The duct is lined by a layer of [[simple columnar epithelium]] resting on a thin [[basement membrane]]. The epithelium is composed primarily of [[principal cells]] and α-intercalated cells.<ref>{{Cite book|title = Color Atlas and Text of Histology|last1 = Gartner|first1 = Leslie|publisher = Lippincott & Wilkins|year = 2014|isbn = 9781451113433|location = Baltimore, MD 21201|pages = 383–399|last2 = Hiatt}}</ref> The [[simple columnar epithelium]] of the collecting duct system transitions into [[urothelium]] near the junction of a papillary duct and a minor calyx.<ref name=":0" />

These cells work in tandem to reabsorb water, sodium, and urea and secrete acid and potassium. The amount of reabsorption or secretion that occurs is related to needs of the body at any given time. These processes are mediated by [[hormones]] ([[aldosterone]], [[vasopressin]]) and the [[osmolarity]] (concentration of electrically charged chemicals) of the surrounding medulla. [[Hormones]] regulate how [[Permeability (earth sciences)|permeable]] the papillary duct is to water and electrolytes. In the medullary collecting duct specifically, [[vasopressin]] upregulates [[urea transporter|urea transporter A1]]. This increases the concentration of urea in the surrounding [[interstitium]] and increases the osmolarity.
[[Osmolarity]] influences the strength of the force that pulls (reabsorbs) water from the papillary duct into the medullary interstitium. This is especially important in the papillary ducts. '''Osmolarity increases''' from the base of the renal pyramid to the apex. It is highest at the renal apex (up to 1200 mOsm). Thus the force driving the reabsorption of water from the collecting system is the greatest in the papillary duct.<ref>{{Cite book|title = Physiology|last = Costanzo|first = Linda|publisher = Wolters Kluwer Health|year = 2011|isbn = 9781451187953|location = Baltimore, MD 21201|pages = 167–172}}</ref>

===Cells===<!--Principal cells redirects here--><!--Intercalated cells redirects here-->
Each component of the collecting duct system contains two cell types, '''intercalated cells''' and a segment-specific cell type:
* For the connecting tubules, this specific cell type is the '''connecting tubule cell'''
* For the collecting ducts, it is the '''principal cell'''. The inner medullary collecting ducts contain an additional cell type, called the '''inner medullary collecting duct cell'''.

====Principal cells====
The principal cell mediates the collecting duct's influence on sodium and potassium balance via [[sodium channel]]s and [[potassium channel]]s located on the cell's [[apical membrane]]. [[Aldosterone]] determines expression of sodium channels (especially the [[ENaC]] on the collecting tubule). Increases in aldosterone increase expression of luminal sodium channels.<ref>{{cite journal |last1= May|first1= Anne|last2= Puoti|first2= Alessandro|last3=Gaeggeler|first3=Hans-Peter|last4=Horisberger|first4=Jean-Daniel|last5=Rossier|first5=Bernard C|date= 1997|title= Early Effect of Aldosterone on the Rate of Synthesis of the Epithelial Sodium Channel a Subunit in A6 Renal Cells|url= http://jasn.asnjournals.org/content/8/12/1813.full.pdf|journal= Journal of the American Society of Nephrology|volume= 8|issue= 12|pages= 1813–1822|doi= 10.1681/ASN.V8121813|pmid= 9402082|access-date= 21 November 2017|doi-access= free}}</ref> Aldosterone also increases the number of [[Na⁺/K⁺-ATPase]] pumps <ref name=GUYTON2006>{{Cite book| edition = 11| publisher = Elsevier Saunders| isbn = 0-7216-0240-1| last = Guyton| first = Arthur C.|author2=John E. Hall| title = Textbook of Medical Physiology| location = Philadelphia| year = 2006}}
</ref>{{rp|949}} that allow increased sodium reabsorption and potassium excretion.<ref name=GUYTON2006 />{{rp|336}} [[Vasopressin]] determines the expression of [[aquaporin]] channels that provide a physical pathway for water to pass through the principal cells.<ref>{{cite journal|doi=10.1007/BF00584753|pmid=2441357|title=Electrophysiological studies in principal cells of rat cortical collecting tubules ADH increases the apical membrane Na+-conductance|year=1987|last1=Schlatter|first1=Eberhard|last2=Schafer|first2=James A.|journal=Pflügers Archiv: European Journal of Physiology|volume=409|issue=1–2|pages=81–92|s2cid=24655136}}</ref> Together, aldosterone and vasopressin let the principal cell control the quantity of water that is reabsorbed.

====Intercalated cells====
[[File:Alpha Intercalated Cell Cartoon.svg|thumbnail|Image depicting an α intercalated cell]]

Intercalated cells come in α, β, and non-α non-β varieties and participate in [[acid–base homeostasis]].<ref>{{Cite journal|last1=Alper|first1=S. L.|last2=Natale|first2=J.|last3=Gluck|first3=S.|last4=Lodish|first4=H. F.|last5=Brown|first5=D.|date=1989-07-01|title=Subtypes of intercalated cells in rat kidney collecting duct defined by antibodies against erythroid band 3 and renal vacuolar H+-ATPase|journal=Proceedings of the National Academy of Sciences|volume=86|issue=14|pages=5429–5433|doi=10.1073/pnas.86.14.5429|issn=0027-8424|pmc=297636|pmid=2526338|bibcode=1989PNAS...86.5429A|doi-access=free}}</ref><ref>{{Cite journal|last1=Kim|first1=J.|last2=Kim|first2=Y. H.|last3=Cha|first3=J. H.|last4=Tisher|first4=C. C.|last5=Madsen|first5=K. M.|date=January 1999|title=Intercalated cell subtypes in connecting tubule and cortical collecting duct of rat and mouse|journal=Journal of the American Society of Nephrology|volume=10|issue=1|pages=1–12|doi=10.1681/ASN.V1011|issn=1046-6673|pmid=9890303|doi-access=free}}</ref>

{| class="wikitable"
! Type of cell !! Secretes !! Reabsorbs
 |-
 | α-intercalated cells ||  [[acid]] (via an apical [[proton pump|H<sup>+</sup>-ATPase]] and [[hydrogen-potassium exchanger|H<sup>+</sup>/K<sup>+</sup> exchanger]]) in the form of [[hydrogen ion]]s || [[bicarbonate]] (via [[band 3]], a basolateral [[chloride-bicarbonate exchanger|Cl<sup>−</sup>/HCO<sub>3</sub><sup>−</sup> exchanger]])<ref>{{cite book| title= Essentials of Human Physiology| first= Thomas M. |last= Nosek| chapter=Section 7/7ch07/7ch07p17 |chapter-url=http://humanphysiology.tuars.com/program/section7/7ch07/7ch07p17.htm |archive-url=https://web.archive.org/web/20160324124828/http://humanphysiology.tuars.com/program/section7/7ch07/7ch07p17.htm|archive-date=2016-03-24}} – "Intercalated Cells"</ref>
 |-
 | β-intercalated cells  || bicarbonate (via [[pendrin]] a specialised apical [[chloride-bicarbonate exchanger|Cl<sup>−</sup>/HCO<sub>3</sub><sup>−</sup>]])
|| acid (via a basal [[proton pump|H<sup>+</sup>-ATPase]])
|-
|non-α non-β intercalated cells
|[[acid]] (via an apical [[proton pump|H<sup>+</sup>-ATPase]] and [[hydrogen-potassium exchanger|H<sup>+</sup>/K<sup>+</sup> exchanger]]) and [[bicarbonate]] (via [[pendrin]])<ref>{{Cite journal|last1=Kim|first1=Young-Hee|last2=Kwon|first2=Tae-Hwan|last3=Frische|first3=Sebastian|last4=Kim|first4=Jin|last5=Tisher|first5=C. Craig|last6=Madsen|first6=Kirsten M.|last7=Nielsen|first7=Søren|date=2002-10-01|title=Immunocytochemical localization of pendrin in intercalated cell subtypes in rat and mouse kidney|journal=American Journal of Physiology. Renal Physiology|volume=283|issue=4|pages=F744–F754|doi=10.1152/ajprenal.00037.2002|pmid=12217866|issn=1931-857X}}</ref><ref>{{Cite journal|last1=Wall|first1=Susan M.|last2=Hassell|first2=Kathryn A.|last3=Royaux|first3=Ines E.|last4=Green|first4=Eric D.|last5=Chang|first5=Judy Y.|last6=Shipley|first6=Gregory L.|last7=Verlander|first7=Jill W.|date=2003-01-01|title=Localization of pendrin in mouse kidney|journal=American Journal of Physiology. Renal Physiology|volume=284|issue=1|pages=F229–F241|doi=10.1152/ajprenal.00147.2002|pmid=12388426|s2cid=22831140|issn=1931-857X}}</ref>
| -
|}

For their contribution to acid–base homeostasis, the intercalated cells play important roles in the kidney's response to [[acidosis]] and [[alkalosis]]. Damage to the α-intercalated cell's ability to secrete acid can result in [[renal tubular acidosis|distal renal tubular acidosis]] (RTA type I, classical RTA)(reference). The intercalated cell population is also extensively modified in response to chronic lithium treatment, including the addition of a largely uncharacterized cell type which expressed markers for both intercalated and principal cells.<ref>{{Cite journal|last1=Christensen|first1=Birgitte Mønster|last2=Marples|first2=David|last3=Kim|first3=Young-Hee|last4=Wang|first4=Weidong|last5=Frøkiær|first5=Jørgen|last6=Nielsen|first6=Søren|date=2004-04-01|title=Changes in cellular composition of kidney collecting duct cells in rats with lithium-induced NDI|journal=American Journal of Physiology. Cell Physiology|volume=286|issue=4|pages=C952–C964|doi=10.1152/ajpcell.00266.2003|pmid=14613889|s2cid=20227998|issn=0363-6143|url=http://pdfs.semanticscholar.org/1276/ef349695561b2405c6e47079975cbdb898d4.pdf|archive-url=https://web.archive.org/web/20190219000744/http://pdfs.semanticscholar.org/1276/ef349695561b2405c6e47079975cbdb898d4.pdf|url-status=dead|archive-date=2019-02-19}}</ref><ref>{{Cite journal|last1=Himmel|first1=Nathaniel J.|last2=Wang|first2=Yirong|last3=Rodriguez|first3=Daniel A.|last4=Sun|first4=Michael A.|last5=Blount|first5=Mitsi A.|date=2018-04-18|title=Chronic lithium treatment induces novel patterns of pendrin localization and expression|journal=American Journal of Physiology. Renal Physiology|volume=315|issue=2|pages=F313–F322|doi=10.1152/ajprenal.00065.2018|issn=1931-857X|pmc=6139525|pmid=29667915}}</ref>