Diuretics and Bone Loss in Rats With Aldosteronism
We hypothesized that the increased urinary Ca2+and Mg2+excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone. Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropri...
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| creator | Law, Peter H. Sun, Yao Bhattacharya, Syamal K. Chhokar, Vikram S. Weber, Karl T. |
| description | We hypothesized that the increased urinary Ca2+and Mg2+excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone.
Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.
In age- and gender-matched, untreated controls, four weeks of aldosterone/salt treatment (ALDO/salt, 0.75 μg/h + 1% NaCl/0.4% KCl in drinking water), four weeks of ALDO/salt + furosemide (40 mg/kg in prepared food), and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-daily gavage), we monitored: 24-h urinary Ca2+and Mg2+excretion; plasma-ionized [Ca2+]o and [Mg2+]o, K+, and parathyroid hormone (PTH); and bone mineral density (BMD) in the femur.
The ALDO/salt increased (p < 0.05) urinary Ca2+and Mg2+excretion (4,969 ± 1,078 and 3,856 ± 440 μg/24 h, respectively) compared with controls (896 ± 138 and 970 ± 137 μg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+and Mg2+excretion (6,976 ± 648 and 6,199 ± 759 μg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental losses (4,003 ± 515 and 3,915 ± 972 μg/24 h). Plasma [Ca2+]o was reduced (p < 0.05) at week 4 ALDO/salt + furosemide and was accompanied by hypokalemia ( |
| doi_str_mv | 10.1016/j.jacc.2005.03.055 |
| format | Article |
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Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.
In age- and gender-matched, untreated controls, four weeks of aldosterone/salt treatment (ALDO/salt, 0.75 μg/h + 1% NaCl/0.4% KCl in drinking water), four weeks of ALDO/salt + furosemide (40 mg/kg in prepared food), and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-daily gavage), we monitored: 24-h urinary Ca2+and Mg2+excretion; plasma-ionized [Ca2+]o and [Mg2+]o, K+, and parathyroid hormone (PTH); and bone mineral density (BMD) in the femur.
The ALDO/salt increased (p < 0.05) urinary Ca2+and Mg2+excretion (4,969 ± 1,078 and 3,856 ± 440 μg/24 h, respectively) compared with controls (896 ± 138 and 970 ± 137 μg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+and Mg2+excretion (6,976 ± 648 and 6,199 ± 759 μg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental losses (4,003 ± 515 and 3,915 ± 972 μg/24 h). Plasma [Ca2+]o was reduced (p < 0.05) at week 4 ALDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol/l) that were rescued by spironolactone. Plasma PTH was increased (p < 0.05) compared with controls (30 ± 4 vs. 11 ± 3 pg/ml, respectively), whereas BMD was decreased (p < 0.05) with ALDO/salt and ALDO/salt + furosemide, but not with spironolactone co-treatment.
In aldosteronism, hypercalciuria and hypermagnesuria and accompanying decrease in plasma-ionized [Ca2+]o and [Mg2+]o lead to hyperparathyroidism that accounts for bone wasting. Furosemide exaggerates these losses, whereas its combination with spironolactone attenuates these responses to prevent bone loss.]]></description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2005.03.055</identifier><identifier>PMID: 15992648</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adrenals. Adrenal axis. Renin-angiotensin system (diseases) ; Animals ; Biological and medical sciences ; Bone density ; Bone Density - drug effects ; Calcium - blood ; Calcium - urine ; Cardiology ; Cardiology. Vascular system ; Disease Models, Animal ; Diseases of the osteoarticular system ; Diuretics - pharmacology ; Endocrinopathies ; Evacuations & rescues ; Food ; Furosemide - pharmacology ; Heart failure ; Hyperaldosteronism - blood ; Hyperaldosteronism - urine ; Magnesium - blood ; Magnesium - urine ; Male ; Medical sciences ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Osteoporosis. Osteomalacia. Paget disease ; Parathyroid Hormone - blood ; Plasma ; Potassium - blood ; Rats ; Rats, Sprague-Dawley ; Rodents ; Salt ; Spironolactone - pharmacology</subject><ispartof>Journal of the American College of Cardiology, 2005-07, Vol.46 (1), p.142-146</ispartof><rights>2005 American College of Cardiology Foundation</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Elsevier Limited Jul 5, 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-5b1fdbf382a31d1f4edf3c6a5b86a054e3d87f04197f0b00e9e0c7fb6ea7a3bf3</citedby><cites>FETCH-LOGICAL-c490t-5b1fdbf382a31d1f4edf3c6a5b86a054e3d87f04197f0b00e9e0c7fb6ea7a3bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109705008661$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17021379$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15992648$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Law, Peter H.</creatorcontrib><creatorcontrib>Sun, Yao</creatorcontrib><creatorcontrib>Bhattacharya, Syamal K.</creatorcontrib><creatorcontrib>Chhokar, Vikram S.</creatorcontrib><creatorcontrib>Weber, Karl T.</creatorcontrib><title>Diuretics and Bone Loss in Rats With Aldosteronism</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description><![CDATA[We hypothesized that the increased urinary Ca2+and Mg2+excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone.
Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.
In age- and gender-matched, untreated controls, four weeks of aldosterone/salt treatment (ALDO/salt, 0.75 μg/h + 1% NaCl/0.4% KCl in drinking water), four weeks of ALDO/salt + furosemide (40 mg/kg in prepared food), and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-daily gavage), we monitored: 24-h urinary Ca2+and Mg2+excretion; plasma-ionized [Ca2+]o and [Mg2+]o, K+, and parathyroid hormone (PTH); and bone mineral density (BMD) in the femur.
The ALDO/salt increased (p < 0.05) urinary Ca2+and Mg2+excretion (4,969 ± 1,078 and 3,856 ± 440 μg/24 h, respectively) compared with controls (896 ± 138 and 970 ± 137 μg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+and Mg2+excretion (6,976 ± 648 and 6,199 ± 759 μg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental losses (4,003 ± 515 and 3,915 ± 972 μg/24 h). Plasma [Ca2+]o was reduced (p < 0.05) at week 4 ALDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol/l) that were rescued by spironolactone. Plasma PTH was increased (p < 0.05) compared with controls (30 ± 4 vs. 11 ± 3 pg/ml, respectively), whereas BMD was decreased (p < 0.05) with ALDO/salt and ALDO/salt + furosemide, but not with spironolactone co-treatment.
In aldosteronism, hypercalciuria and hypermagnesuria and accompanying decrease in plasma-ionized [Ca2+]o and [Mg2+]o lead to hyperparathyroidism that accounts for bone wasting. Furosemide exaggerates these losses, whereas its combination with spironolactone attenuates these responses to prevent bone loss.]]></description><subject>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone density</subject><subject>Bone Density - drug effects</subject><subject>Calcium - blood</subject><subject>Calcium - urine</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Disease Models, Animal</subject><subject>Diseases of the osteoarticular system</subject><subject>Diuretics - pharmacology</subject><subject>Endocrinopathies</subject><subject>Evacuations & rescues</subject><subject>Food</subject><subject>Furosemide - pharmacology</subject><subject>Heart failure</subject><subject>Hyperaldosteronism - blood</subject><subject>Hyperaldosteronism - urine</subject><subject>Magnesium - blood</subject><subject>Magnesium - urine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Parathyroid Hormone - blood</subject><subject>Plasma</subject><subject>Potassium - blood</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Salt</subject><subject>Spironolactone - pharmacology</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoMo7uzqH_AgDaK3bqs6naQDXnbX9QMGBFE8hnRSwTQ93WvSLfjvzTADCx68VF2e96XqYewFQoOA8u3YjNa5pgUQDfAGhHjEdihEX3Oh1WO2A8VFjaDVBbvMeQQA2aN-yi5QaN3Krt-x9n3cEq3R5crOvrpZZqr2S85VnKuvds3Vj7j-rK4nv-SV0jLHfHjGngQ7ZXp-3lfs-4e7b7ef6v2Xj59vr_e16zSstRgw-CHwvrUcPYaOfOBOWjH00oLoiPteBehQlzkAkCZwKgySrLK8BK_Ym1PvfVp-bZRXc4jZ0TTZmZYtG6m0VthjAV_9A47LluZym0EBEmUnZV-o9kS5VP5LFMx9igeb_hgEc_RpRnP0aY4-DXBTfJbQy3P1NhzIP0TOAgvw-gzY7OwUkp1dzA-cgha50oV7d-KoGPsdKZnsIs2OfEzkVuOX-L87_gL3pZHk</recordid><startdate>20050705</startdate><enddate>20050705</enddate><creator>Law, Peter H.</creator><creator>Sun, Yao</creator><creator>Bhattacharya, Syamal K.</creator><creator>Chhokar, Vikram S.</creator><creator>Weber, Karl T.</creator><general>Elsevier Inc</general><general>Elsevier Science</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20050705</creationdate><title>Diuretics and Bone Loss in Rats With Aldosteronism</title><author>Law, Peter H. ; Sun, Yao ; Bhattacharya, Syamal K. ; Chhokar, Vikram S. ; Weber, Karl T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-5b1fdbf382a31d1f4edf3c6a5b86a054e3d87f04197f0b00e9e0c7fb6ea7a3bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone density</topic><topic>Bone Density - drug effects</topic><topic>Calcium - blood</topic><topic>Calcium - urine</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Disease Models, Animal</topic><topic>Diseases of the osteoarticular system</topic><topic>Diuretics - pharmacology</topic><topic>Endocrinopathies</topic><topic>Evacuations & rescues</topic><topic>Food</topic><topic>Furosemide - pharmacology</topic><topic>Heart failure</topic><topic>Hyperaldosteronism - blood</topic><topic>Hyperaldosteronism - urine</topic><topic>Magnesium - blood</topic><topic>Magnesium - urine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Osteoporosis. Osteomalacia. Paget disease</topic><topic>Parathyroid Hormone - blood</topic><topic>Plasma</topic><topic>Potassium - blood</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Salt</topic><topic>Spironolactone - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Law, Peter H.</creatorcontrib><creatorcontrib>Sun, Yao</creatorcontrib><creatorcontrib>Bhattacharya, Syamal K.</creatorcontrib><creatorcontrib>Chhokar, Vikram S.</creatorcontrib><creatorcontrib>Weber, Karl T.</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>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Law, Peter H.</au><au>Sun, Yao</au><au>Bhattacharya, Syamal K.</au><au>Chhokar, Vikram S.</au><au>Weber, Karl T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diuretics and Bone Loss in Rats With Aldosteronism</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2005-07-05</date><risdate>2005</risdate><volume>46</volume><issue>1</issue><spage>142</spage><epage>146</epage><pages>142-146</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract><![CDATA[We hypothesized that the increased urinary Ca2+and Mg2+excretion and bone loss that accompanies aldosteronism is aggravated with furosemide and is attenuated by spironolactone.
Furosemide, a loop diuretic, is commonly used in patients with congestive heart failure (CHF), in which chronic, inappropriate (dietary Na+) elevations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.
In age- and gender-matched, untreated controls, four weeks of aldosterone/salt treatment (ALDO/salt, 0.75 μg/h + 1% NaCl/0.4% KCl in drinking water), four weeks of ALDO/salt + furosemide (40 mg/kg in prepared food), and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-daily gavage), we monitored: 24-h urinary Ca2+and Mg2+excretion; plasma-ionized [Ca2+]o and [Mg2+]o, K+, and parathyroid hormone (PTH); and bone mineral density (BMD) in the femur.
The ALDO/salt increased (p < 0.05) urinary Ca2+and Mg2+excretion (4,969 ± 1,078 and 3,856 ± 440 μg/24 h, respectively) compared with controls (896 ± 138 and 970 ± 137 μg/24 h, respectively); furosemide co-treatment further increased (p < 0.05) urinary Ca2+and Mg2+excretion (6,976 ± 648 and 6,199 ± 759 μg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these incremental losses (4,003 ± 515 and 3,915 ± 972 μg/24 h). Plasma [Ca2+]o was reduced (p < 0.05) at week 4 ALDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol/l) that were rescued by spironolactone. Plasma PTH was increased (p < 0.05) compared with controls (30 ± 4 vs. 11 ± 3 pg/ml, respectively), whereas BMD was decreased (p < 0.05) with ALDO/salt and ALDO/salt + furosemide, but not with spironolactone co-treatment.
In aldosteronism, hypercalciuria and hypermagnesuria and accompanying decrease in plasma-ionized [Ca2+]o and [Mg2+]o lead to hyperparathyroidism that accounts for bone wasting. Furosemide exaggerates these losses, whereas its combination with spironolactone attenuates these responses to prevent bone loss.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15992648</pmid><doi>10.1016/j.jacc.2005.03.055</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenals. Adrenal axis. Renin-angiotensin system (diseases) Animals Biological and medical sciences Bone density Bone Density - drug effects Calcium - blood Calcium - urine Cardiology Cardiology. Vascular system Disease Models, Animal Diseases of the osteoarticular system Diuretics - pharmacology Endocrinopathies Evacuations & rescues Food Furosemide - pharmacology Heart failure Hyperaldosteronism - blood Hyperaldosteronism - urine Magnesium - blood Magnesium - urine Male Medical sciences Non tumoral diseases. Target tissue resistance. Benign neoplasms Osteoporosis. Osteomalacia. Paget disease Parathyroid Hormone - blood Plasma Potassium - blood Rats Rats, Sprague-Dawley Rodents Salt Spironolactone - pharmacology |
| title | Diuretics and Bone Loss in Rats With Aldosteronism |
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