High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure
High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure. Calcium salts are used as phosphate binders in renal failure, while high calcium diet also improves vasorelaxation and enhances natriuresis. The influences of calcium intake on renal renin-angiotensi...
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creator | Pörsti, Ilkka Fan, Meng Kööbi, Peeter Jolma, Pasi Kalliovalkama, Jarkko Vehmas, Tuija I. Helin, Heikki Holthöfer, Harry Mervaala, Eero Nyman, Tuulikki Tikkanen, Ilkka |
description | High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure.
Calcium salts are used as phosphate binders in renal failure, while high calcium diet also improves vasorelaxation and enhances natriuresis. The influences of calcium intake on renal renin-angiotensin system (RAS) are largely unknown.
Four weeks after NTX, rats were put on 3.0% or 0.3% calcium diet for 8 weeks (12-week study). In additional experiments, 15 weeks after NTX, rats were put on similar diets for 12 weeks (27-week study). Appropriate blood, urine, and kidney samples were taken. Renal angiotensin-converting enzyme (ACE) and angiotensin II receptors (AT1, AT2) were examined using autoradiography, ACE also using Western blotting, and connective tissue growth factor (CTGF) using immunohistochemistry.
In the 12-week study, albuminuria increased 5-fold in NTX rats, but only 2-fold in calcium NTX rats on 3.0% calcium. In the 27-week study, high calcium intake decreased blood pressure, retarded progression of renal failure, reduced glomerulosclerosis, interstitial damage, and aortic calcifications, and improved survival from 50% to 92% in NTX rats. In both experiments plasma parathyroid hormone and phosphate were elevated after NTX, and suppressed by high calcium diet, while kidney ACE was down-regulated by 40% or more after increased calcium intake. In the 27-week study renal CTGF was decreased and cortical AT1 receptor density reduced after high calcium diet.
High calcium diet down-regulated kidney ACE, reduced albuminuria and blood pressure, and favorably influenced kidney morphology in experimental renal failure. These findings suggest a link between calcium metabolism and kidney ACE expression, which may play a role in the progression of renal damage. |
doi_str_mv | 10.1111/j.1523-1755.2004.66006.x |
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Calcium salts are used as phosphate binders in renal failure, while high calcium diet also improves vasorelaxation and enhances natriuresis. The influences of calcium intake on renal renin-angiotensin system (RAS) are largely unknown.
Four weeks after NTX, rats were put on 3.0% or 0.3% calcium diet for 8 weeks (12-week study). In additional experiments, 15 weeks after NTX, rats were put on similar diets for 12 weeks (27-week study). Appropriate blood, urine, and kidney samples were taken. Renal angiotensin-converting enzyme (ACE) and angiotensin II receptors (AT1, AT2) were examined using autoradiography, ACE also using Western blotting, and connective tissue growth factor (CTGF) using immunohistochemistry.
In the 12-week study, albuminuria increased 5-fold in NTX rats, but only 2-fold in calcium NTX rats on 3.0% calcium. In the 27-week study, high calcium intake decreased blood pressure, retarded progression of renal failure, reduced glomerulosclerosis, interstitial damage, and aortic calcifications, and improved survival from 50% to 92% in NTX rats. In both experiments plasma parathyroid hormone and phosphate were elevated after NTX, and suppressed by high calcium diet, while kidney ACE was down-regulated by 40% or more after increased calcium intake. In the 27-week study renal CTGF was decreased and cortical AT1 receptor density reduced after high calcium diet.
High calcium diet down-regulated kidney ACE, reduced albuminuria and blood pressure, and favorably influenced kidney morphology in experimental renal failure. These findings suggest a link between calcium metabolism and kidney ACE expression, which may play a role in the progression of renal damage.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1111/j.1523-1755.2004.66006.x</identifier><identifier>PMID: 15569305</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Albuminuria - drug therapy ; Albuminuria - metabolism ; Albuminuria - pathology ; angiotensin-converting enzyme ; Animals ; Aorta - pathology ; Biological and medical sciences ; calcium diet ; Calcium, Dietary - pharmacology ; Connective Tissue Growth Factor ; Down-Regulation - drug effects ; Immediate-Early Proteins - metabolism ; Intercellular Signaling Peptides and Proteins - metabolism ; Kidney - enzymology ; Kidney - pathology ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; parathyroid hormone ; Parathyroid Hormone - blood ; Peptidyl-Dipeptidase A - metabolism ; phosphate ; Phosphates - blood ; Rats ; Rats, Sprague-Dawley ; Renal failure ; Renal Insufficiency - drug therapy ; Renal Insufficiency - metabolism ; Renal Insufficiency - pathology ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology</subject><ispartof>Kidney international, 2004-12, Vol.66 (6), p.2155-2166</ispartof><rights>2004 International Society of Nephrology</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-19e4edd01bbb136e8563687afd8f6deb2479de7292102af52edc1617e0070aac3</citedby><cites>FETCH-LOGICAL-c532t-19e4edd01bbb136e8563687afd8f6deb2479de7292102af52edc1617e0070aac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210108890?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16330779$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15569305$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pörsti, Ilkka</creatorcontrib><creatorcontrib>Fan, Meng</creatorcontrib><creatorcontrib>Kööbi, Peeter</creatorcontrib><creatorcontrib>Jolma, Pasi</creatorcontrib><creatorcontrib>Kalliovalkama, Jarkko</creatorcontrib><creatorcontrib>Vehmas, Tuija I.</creatorcontrib><creatorcontrib>Helin, Heikki</creatorcontrib><creatorcontrib>Holthöfer, Harry</creatorcontrib><creatorcontrib>Mervaala, Eero</creatorcontrib><creatorcontrib>Nyman, Tuulikki</creatorcontrib><creatorcontrib>Tikkanen, Ilkka</creatorcontrib><title>High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure.
Calcium salts are used as phosphate binders in renal failure, while high calcium diet also improves vasorelaxation and enhances natriuresis. The influences of calcium intake on renal renin-angiotensin system (RAS) are largely unknown.
Four weeks after NTX, rats were put on 3.0% or 0.3% calcium diet for 8 weeks (12-week study). In additional experiments, 15 weeks after NTX, rats were put on similar diets for 12 weeks (27-week study). Appropriate blood, urine, and kidney samples were taken. Renal angiotensin-converting enzyme (ACE) and angiotensin II receptors (AT1, AT2) were examined using autoradiography, ACE also using Western blotting, and connective tissue growth factor (CTGF) using immunohistochemistry.
In the 12-week study, albuminuria increased 5-fold in NTX rats, but only 2-fold in calcium NTX rats on 3.0% calcium. In the 27-week study, high calcium intake decreased blood pressure, retarded progression of renal failure, reduced glomerulosclerosis, interstitial damage, and aortic calcifications, and improved survival from 50% to 92% in NTX rats. In both experiments plasma parathyroid hormone and phosphate were elevated after NTX, and suppressed by high calcium diet, while kidney ACE was down-regulated by 40% or more after increased calcium intake. In the 27-week study renal CTGF was decreased and cortical AT1 receptor density reduced after high calcium diet.
High calcium diet down-regulated kidney ACE, reduced albuminuria and blood pressure, and favorably influenced kidney morphology in experimental renal failure. These findings suggest a link between calcium metabolism and kidney ACE expression, which may play a role in the progression of renal damage.</description><subject>Albuminuria - drug therapy</subject><subject>Albuminuria - metabolism</subject><subject>Albuminuria - pathology</subject><subject>angiotensin-converting enzyme</subject><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Biological and medical sciences</subject><subject>calcium diet</subject><subject>Calcium, Dietary - pharmacology</subject><subject>Connective Tissue Growth Factor</subject><subject>Down-Regulation - drug effects</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Kidney - enzymology</subject><subject>Kidney - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>parathyroid hormone</subject><subject>Parathyroid Hormone - blood</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>phosphate</subject><subject>Phosphates - blood</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal failure</subject><subject>Renal Insufficiency - drug therapy</subject><subject>Renal Insufficiency - metabolism</subject><subject>Renal Insufficiency - pathology</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkUtv1DAUhS1ERacDPwFkIZVdgh-xnSyhKhSpEhtYW459M3hInMFOygy_HqczaqVu6oUfut-9Oj4HIUxJSfP6uC2pYLygSoiSEVKVUhIiy_0LtHoovEQrQmpRMMHrc3SR0pbkd8PJK3ROhZD5JlbI3vjNL2xNb_08YOdhwm78G4oIm7k3EyT827sAB2zCxo8ThORDYcdwB3HyYYMh_DsMgH3AsN9B9AOEyfQ4Qsh7Z3w_R3iNzjrTJ3hzOtfo55frH1c3xe33r9-uPt0WVnA2FbSBCpwjtG1byiXUQnJZK9O5upMOWlapxoFiDaOEmU4wcJZKqoAQRYyxfI0-HOfu4vhnhjTpwScLfW8CjHPSUlGePRDPglRxRprs1Rq9fwJuxznmryWdRVBS1w3JUH2EbBxTitDpXfbBxIOmRC9x6a1eUtFLKnqJS9_Hpfe59d1p_twO4B4bT_lk4PIEmJRD6qIJ1qdHTnJOlFqEvj1ywUzZ8QegqpqqVjLXPx_rkP2_8xB1sh6CBecj2Em70T-v9j_4fr4e</recordid><startdate>20041201</startdate><enddate>20041201</enddate><creator>Pörsti, Ilkka</creator><creator>Fan, Meng</creator><creator>Kööbi, Peeter</creator><creator>Jolma, Pasi</creator><creator>Kalliovalkama, Jarkko</creator><creator>Vehmas, Tuija I.</creator><creator>Helin, Heikki</creator><creator>Holthöfer, Harry</creator><creator>Mervaala, Eero</creator><creator>Nyman, Tuulikki</creator><creator>Tikkanen, Ilkka</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20041201</creationdate><title>High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure</title><author>Pörsti, Ilkka ; Fan, Meng ; Kööbi, Peeter ; Jolma, Pasi ; Kalliovalkama, Jarkko ; Vehmas, Tuija I. ; Helin, Heikki ; Holthöfer, Harry ; Mervaala, Eero ; Nyman, Tuulikki ; Tikkanen, Ilkka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-19e4edd01bbb136e8563687afd8f6deb2479de7292102af52edc1617e0070aac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Albuminuria - drug therapy</topic><topic>Albuminuria - metabolism</topic><topic>Albuminuria - pathology</topic><topic>angiotensin-converting enzyme</topic><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Biological and medical sciences</topic><topic>calcium diet</topic><topic>Calcium, Dietary - pharmacology</topic><topic>Connective Tissue Growth Factor</topic><topic>Down-Regulation - drug effects</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Kidney - enzymology</topic><topic>Kidney - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>parathyroid hormone</topic><topic>Parathyroid Hormone - blood</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>phosphate</topic><topic>Phosphates - blood</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal failure</topic><topic>Renal Insufficiency - drug therapy</topic><topic>Renal Insufficiency - metabolism</topic><topic>Renal Insufficiency - pathology</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pörsti, Ilkka</creatorcontrib><creatorcontrib>Fan, Meng</creatorcontrib><creatorcontrib>Kööbi, Peeter</creatorcontrib><creatorcontrib>Jolma, Pasi</creatorcontrib><creatorcontrib>Kalliovalkama, Jarkko</creatorcontrib><creatorcontrib>Vehmas, Tuija I.</creatorcontrib><creatorcontrib>Helin, Heikki</creatorcontrib><creatorcontrib>Holthöfer, Harry</creatorcontrib><creatorcontrib>Mervaala, Eero</creatorcontrib><creatorcontrib>Nyman, Tuulikki</creatorcontrib><creatorcontrib>Tikkanen, Ilkka</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pörsti, Ilkka</au><au>Fan, Meng</au><au>Kööbi, Peeter</au><au>Jolma, Pasi</au><au>Kalliovalkama, Jarkko</au><au>Vehmas, Tuija I.</au><au>Helin, Heikki</au><au>Holthöfer, Harry</au><au>Mervaala, Eero</au><au>Nyman, Tuulikki</au><au>Tikkanen, Ilkka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2004-12-01</date><risdate>2004</risdate><volume>66</volume><issue>6</issue><spage>2155</spage><epage>2166</epage><pages>2155-2166</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure.
Calcium salts are used as phosphate binders in renal failure, while high calcium diet also improves vasorelaxation and enhances natriuresis. The influences of calcium intake on renal renin-angiotensin system (RAS) are largely unknown.
Four weeks after NTX, rats were put on 3.0% or 0.3% calcium diet for 8 weeks (12-week study). In additional experiments, 15 weeks after NTX, rats were put on similar diets for 12 weeks (27-week study). Appropriate blood, urine, and kidney samples were taken. Renal angiotensin-converting enzyme (ACE) and angiotensin II receptors (AT1, AT2) were examined using autoradiography, ACE also using Western blotting, and connective tissue growth factor (CTGF) using immunohistochemistry.
In the 12-week study, albuminuria increased 5-fold in NTX rats, but only 2-fold in calcium NTX rats on 3.0% calcium. In the 27-week study, high calcium intake decreased blood pressure, retarded progression of renal failure, reduced glomerulosclerosis, interstitial damage, and aortic calcifications, and improved survival from 50% to 92% in NTX rats. In both experiments plasma parathyroid hormone and phosphate were elevated after NTX, and suppressed by high calcium diet, while kidney ACE was down-regulated by 40% or more after increased calcium intake. In the 27-week study renal CTGF was decreased and cortical AT1 receptor density reduced after high calcium diet.
High calcium diet down-regulated kidney ACE, reduced albuminuria and blood pressure, and favorably influenced kidney morphology in experimental renal failure. These findings suggest a link between calcium metabolism and kidney ACE expression, which may play a role in the progression of renal damage.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15569305</pmid><doi>10.1111/j.1523-1755.2004.66006.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Albuminuria - drug therapy Albuminuria - metabolism Albuminuria - pathology angiotensin-converting enzyme Animals Aorta - pathology Biological and medical sciences calcium diet Calcium, Dietary - pharmacology Connective Tissue Growth Factor Down-Regulation - drug effects Immediate-Early Proteins - metabolism Intercellular Signaling Peptides and Proteins - metabolism Kidney - enzymology Kidney - pathology Male Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure parathyroid hormone Parathyroid Hormone - blood Peptidyl-Dipeptidase A - metabolism phosphate Phosphates - blood Rats Rats, Sprague-Dawley Renal failure Renal Insufficiency - drug therapy Renal Insufficiency - metabolism Renal Insufficiency - pathology Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology |
title | High calcium diet down-regulates kidney angiotensin-converting enzyme in experimental renal failure |
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