Angiotensin II and Renal Tubular Ion Transport
Angiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. In ad...
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2005-01-01
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Series: | The Scientific World Journal |
Online Access: | http://dx.doi.org/10.1100/tsw.2005.92 |
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author | Patricia Valles Jan Wysocki Daniel Batlle |
author_facet | Patricia Valles Jan Wysocki Daniel Batlle |
author_sort | Patricia Valles |
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description | Angiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. In addition, angiotensin II stimulates H+ secretion and HCO3– reabsorption in both proximal and distal tubules and regulates H+-ATPase activity in intercalated cells of the collecting tubule.
Different results regarding the effect of angiotensin II on bicarbonate reabsorption and proton secretion have been reported at the functional level, depending on the angiotensin II concentration and tubule segment studied. It is likely that interstitial angiotensin II is more important in regulating hemodynamic and transport functions than circulating angiotensin II. In proximal tubules, stimulation of bicarbonate reabsorption, Na+/H+-exchange, and Na+/HCO3– cotransport has been found using low concentrations (<10–9M), while inhibition of bicarbonate reabsorption has been documented using concentrations higher than 10–8M.
Evidence for the regulation of H+-ATPase activity in vivo and in vitro by trafficking/exocytosis has been provided. An additional level of H+-ATPase regulation via protein synthesis may be important as well. Recently, we have shown that both aldosterone and angiotensin II provide such a mechanism of regulation in vivo at the level of the medullary collecting tubule. Interestingly, in this part of the nephron, the effects of aldosterone and angiotensin II are not sodium dependent, whereas in the cortical collecting duct, both aldosterone and angiotensin II, by contrast, affect H+ secretion by sodium-dependent mechanisms. |
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institution | Kabale University |
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language | English |
publishDate | 2005-01-01 |
publisher | Wiley |
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series | The Scientific World Journal |
spelling | doaj-art-0e7756aead0a4029bd273a46672104142025-02-03T05:50:15ZengWileyThe Scientific World Journal1537-744X2005-01-01568069010.1100/tsw.2005.92Angiotensin II and Renal Tubular Ion TransportPatricia Valles0Jan Wysocki1Daniel Batlle2Area de Fisiopatología, Departamento de Patología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, ArgentinaDivision of Nephrology and Hypertension, Department of Medicine, Northwestern University, The Feinberg School of Medicine, Chicago, USADivision of Nephrology and Hypertension, Department of Medicine, Northwestern University, The Feinberg School of Medicine, Chicago, USAAngiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. In addition, angiotensin II stimulates H+ secretion and HCO3– reabsorption in both proximal and distal tubules and regulates H+-ATPase activity in intercalated cells of the collecting tubule. Different results regarding the effect of angiotensin II on bicarbonate reabsorption and proton secretion have been reported at the functional level, depending on the angiotensin II concentration and tubule segment studied. It is likely that interstitial angiotensin II is more important in regulating hemodynamic and transport functions than circulating angiotensin II. In proximal tubules, stimulation of bicarbonate reabsorption, Na+/H+-exchange, and Na+/HCO3– cotransport has been found using low concentrations (<10–9M), while inhibition of bicarbonate reabsorption has been documented using concentrations higher than 10–8M. Evidence for the regulation of H+-ATPase activity in vivo and in vitro by trafficking/exocytosis has been provided. An additional level of H+-ATPase regulation via protein synthesis may be important as well. Recently, we have shown that both aldosterone and angiotensin II provide such a mechanism of regulation in vivo at the level of the medullary collecting tubule. Interestingly, in this part of the nephron, the effects of aldosterone and angiotensin II are not sodium dependent, whereas in the cortical collecting duct, both aldosterone and angiotensin II, by contrast, affect H+ secretion by sodium-dependent mechanisms.http://dx.doi.org/10.1100/tsw.2005.92 |
spellingShingle | Patricia Valles Jan Wysocki Daniel Batlle Angiotensin II and Renal Tubular Ion Transport The Scientific World Journal |
title | Angiotensin II and Renal Tubular Ion Transport |
title_full | Angiotensin II and Renal Tubular Ion Transport |
title_fullStr | Angiotensin II and Renal Tubular Ion Transport |
title_full_unstemmed | Angiotensin II and Renal Tubular Ion Transport |
title_short | Angiotensin II and Renal Tubular Ion Transport |
title_sort | angiotensin ii and renal tubular ion transport |
url | http://dx.doi.org/10.1100/tsw.2005.92 |
work_keys_str_mv | AT patriciavalles angiotensiniiandrenaltubulariontransport AT janwysocki angiotensiniiandrenaltubulariontransport AT danielbatlle angiotensiniiandrenaltubulariontransport |