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Endothelins: vasoactive modulators of renal function in health and disease
Vasoactive autocoids with directly opposing actions on the renal vasculature, glomerular function, and in salt and water homeostasis have been demonstrated in the kidney. In the renal cortex, endothelin (ET)-1 and angiotensin-II cause vasoconstriction, decreasing renal blood flow, and glomerular fil...
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| Published in: | Pharmacology & therapeutics (Oxford) 2001-04, Vol.90 (1), p.61-88 |
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| Main Authors: | , |
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| container_end_page | 88 |
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| container_title | Pharmacology & therapeutics (Oxford) |
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| creator | Naicker, Sarala Bhoola, Kanti D |
| description | Vasoactive autocoids with directly opposing actions on the renal vasculature, glomerular function, and in salt and water homeostasis have been demonstrated in the kidney. In the renal cortex, endothelin (ET)-1 and angiotensin-II cause vasoconstriction, decreasing renal blood flow, and glomerular filtration rate, whereas bradykinin and atrial natriuretic peptide cause vasodilation and increase glomerular capillary permeability. ET-1 causes vasoconstriction of the afferent and efferent arteries and outer medullary descending vasa recta, thereby decreasing vasa recta and papillary blood flow, while bradykinin has the opposite effect. ET-1 stimulates cell proliferation, increasing the expression of several genes, including collagenase, prostaglandin endoperoxidase synthase, and platelet-derived growth factor. ET-1 promotes natriuresis via the ET-B receptor, causing down-regulation of the epithelial Na
+ channel in the renal tubule. Thus, ETs affect three major aspects of renal physiology: vascular and mesangial tone, Na
+ and water excretion, and cell proliferation and matrix formation. |
| doi_str_mv | 10.1016/S0163-7258(01)00131-0 |
| format | article |
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+ channel in the renal tubule. Thus, ETs affect three major aspects of renal physiology: vascular and mesangial tone, Na
+ and water excretion, and cell proliferation and matrix formation.</description><subject>Acute transplant rejection</subject><subject>Animals</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Endothelin genes</subject><subject>Endothelin receptors</subject><subject>Endothelin-1</subject><subject>Endothelins - genetics</subject><subject>Endothelins - metabolism</subject><subject>Endothelins - physiology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Glomerular disease</subject><subject>Humans</subject><subject>Kidney - blood supply</subject><subject>Kidney - pathology</subject><subject>Kidney - physiology</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - physiopathology</subject><subject>Microscopy, Confocal</subject><subject>Models, Chemical</subject><subject>Models, Molecular</subject><subject>Receptors, Endothelin - chemistry</subject><subject>Receptors, Endothelin - genetics</subject><subject>Receptors, Endothelin - metabolism</subject><subject>Renin-Angiotensin System</subject><subject>Signal Transduction</subject><issn>0163-7258</issn><issn>1879-016X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNqFkD1PwzAQhi0EoqXwE0CeEAyBc-IkhgWhqnypEgMd2CzHvqhGiQ12Uol_T_ohGFnuhnveO91DyCmDKwasuH4bSpaUaS4ugF0CsIwlsEfGTJQ3yTB73yfjX2REjmL8AADOIT0kI8Y4F2VajMnLzBnfLbGxLt7SlYpe6c6ukLbe9I3qfIjU1zSgUw2tezcMvaPW0SWqpltS5Qw1NqKKeEwOatVEPNn1CVk8zBbTp2T--vg8vZ8nOitYl1SF5ghcCExZrqBEkeccGdcaa4V1KiDTNdemylNI0wwKKIxhqMs8q3Khswk53679DP6rx9jJ1kaNTaMc-j7KctADTIgBzLegDj7GgLX8DLZV4VsykGuHcuNQrgVJYHLjUMKQO9sd6KsWzV9qJ20A7rYADl-uLAYZtUWn0diAupPG239O_AD7b4Eh</recordid><startdate>20010401</startdate><enddate>20010401</enddate><creator>Naicker, Sarala</creator><creator>Bhoola, Kanti D</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20010401</creationdate><title>Endothelins: vasoactive modulators of renal function in health and disease</title><author>Naicker, Sarala ; Bhoola, Kanti D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-b6c4e0488e215a07e8554e14ccefaef2803cf4cdb5202230606dd1ec753b58c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acute transplant rejection</topic><topic>Animals</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Endothelin genes</topic><topic>Endothelin receptors</topic><topic>Endothelin-1</topic><topic>Endothelins - genetics</topic><topic>Endothelins - metabolism</topic><topic>Endothelins - physiology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Glomerular disease</topic><topic>Humans</topic><topic>Kidney - blood supply</topic><topic>Kidney - pathology</topic><topic>Kidney - physiology</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - physiopathology</topic><topic>Microscopy, Confocal</topic><topic>Models, Chemical</topic><topic>Models, Molecular</topic><topic>Receptors, Endothelin - chemistry</topic><topic>Receptors, Endothelin - genetics</topic><topic>Receptors, Endothelin - metabolism</topic><topic>Renin-Angiotensin System</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Naicker, Sarala</creatorcontrib><creatorcontrib>Bhoola, Kanti D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pharmacology & therapeutics (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Naicker, Sarala</au><au>Bhoola, Kanti D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelins: vasoactive modulators of renal function in health and disease</atitle><jtitle>Pharmacology & therapeutics (Oxford)</jtitle><addtitle>Pharmacol Ther</addtitle><date>2001-04-01</date><risdate>2001</risdate><volume>90</volume><issue>1</issue><spage>61</spage><epage>88</epage><pages>61-88</pages><issn>0163-7258</issn><eissn>1879-016X</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>Vasoactive autocoids with directly opposing actions on the renal vasculature, glomerular function, and in salt and water homeostasis have been demonstrated in the kidney. In the renal cortex, endothelin (ET)-1 and angiotensin-II cause vasoconstriction, decreasing renal blood flow, and glomerular filtration rate, whereas bradykinin and atrial natriuretic peptide cause vasodilation and increase glomerular capillary permeability. ET-1 causes vasoconstriction of the afferent and efferent arteries and outer medullary descending vasa recta, thereby decreasing vasa recta and papillary blood flow, while bradykinin has the opposite effect. ET-1 stimulates cell proliferation, increasing the expression of several genes, including collagenase, prostaglandin endoperoxidase synthase, and platelet-derived growth factor. ET-1 promotes natriuresis via the ET-B receptor, causing down-regulation of the epithelial Na
+ channel in the renal tubule. Thus, ETs affect three major aspects of renal physiology: vascular and mesangial tone, Na
+ and water excretion, and cell proliferation and matrix formation.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>11448726</pmid><doi>10.1016/S0163-7258(01)00131-0</doi><tpages>28</tpages></addata></record> |
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| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | Acute transplant rejection Animals Atrial Natriuretic Factor - metabolism Endothelin genes Endothelin receptors Endothelin-1 Endothelins - genetics Endothelins - metabolism Endothelins - physiology Endothelium, Vascular - metabolism Gene Expression Regulation Glomerular disease Humans Kidney - blood supply Kidney - pathology Kidney - physiology Kidney Diseases - metabolism Kidney Diseases - physiopathology Microscopy, Confocal Models, Chemical Models, Molecular Receptors, Endothelin - chemistry Receptors, Endothelin - genetics Receptors, Endothelin - metabolism Renin-Angiotensin System Signal Transduction |
| title | Endothelins: vasoactive modulators of renal function in health and disease |
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