Angiotensin II activates H+‐ATPase in type A intercalated cells in mouse cortical collecting duct

Pech, Vladimir; Zheng, Wencui; Pham, Truyen D.; Verlander, Jill W.; Wall, Susan M.

doi:10.1096/fasebj.21.6.a1329-a

Cited by 1 publication

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“…In CCDs perfused in vitro, angiotensin II increases ENaC-mediated Na + absorption, 99 which should increase the lumen-negative voltage, V T . However, since angiotensin II application did not change transepithelial voltage, V T , 25,97 movement of a counter ion may shunt this ENaC-mediated current. The increased H + secretion that follows angiotensin II application may provide such a counter ion.…”

Section: Role Of Pendrin In Na+ and K+ Balancementioning

confidence: 86%

“…The increased H + secretion that follows angiotensin II application may provide such a counter ion. 97,100 In CCDs perfused in vitro, this lumen-negative V T increases with the application of H + -ATPase inhibitors to the perfusate 100 but falls with ENaC inhibitors. 14,19 Since angiotensin II increases both H + secretion and Na + absorption in mouse CCDs, movement of these 2 ions may shunt the voltage generated by transport of the other.…”

Section: Role Of Pendrin In Na+ and K+ Balancementioning

confidence: 97%

“…However, in type A ICs, it increased both apical plasma membrane H + -ATPase abundance and HCO 3 − absorption, which reflects increased H + secretion. 97,98…”

Section: Role Of Pendrin In Na+ and K+ Balancementioning

confidence: 99%

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Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020

Wall

2022

Hypertension

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Intercalated cells make up about a third of all cells within the connecting tubule and the collecting duct and are subclassified as type A, type B and non-A, non-B based on the subcellular distribution of the H + -ATPase, which dictates whether it secretes H + or HCO 3 − . Type B intercalated cells mediate Cl − absorption and HCO 3 − secretion, which occurs largely through the anion exchanger pendrin. Pendrin is stimulated by angiotensin II via the angiotensin type 1a receptor and by aldosterone through MR (mineralocorticoid receptor). Aldosterone stimulates pendrin expression and function, in part, through the alkalosis it generates. Pendrin-mediated HCO 3 − secretion increases in models of metabolic alkalosis, which attenuates the alkalosis. However, pendrin-positive intercalated cells also regulate blood pressure, at least partly, through pendrin-mediated Cl − absorption and through their indirect effect on the epithelial Na + channel, ENaC. This aldosterone-induced increase in pendrin secondarily stimulates ENaC, thereby contributing to the aldosterone pressor response. This review describes the contribution of pendrin-positive intercalated cells to Na + , K + , Cl − and acid-base balance.

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Section: Role Of Pendrin In Na+ and K+ Balancementioning

confidence: 86%