Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat
The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm–Horsfall protein (THP) secretion. Three groups of male Sprague–Dawley rats were studied: (A) diabetic ra...
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| Veröffentlicht in: | Journal of diabetes and its complications 2000, Vol.14 (1), p.46-52 |
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| creator | Thorup, Christian Ollerstam, Anna Persson, A.Erik G Torffvit, Ole |
| description | The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm–Horsfall protein (THP) secretion. Three groups of male Sprague–Dawley rats were studied: (A) diabetic rats with blood glucose levels (BG) |
| doi_str_mv | 10.1016/S1056-8727(00)00056-8 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71262618</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1056872700000568</els_id><sourcerecordid>71262618</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-fdeae3a58fc3a689060372c30bfbe06ee80f3de87f2a0b0d02103da63ed7e6f53</originalsourceid><addsrcrecordid>eNqFkEtP3TAQRi1UxLM_oZUXVUUXKeOYOLkrhFBbkBAsaKXurIk9Lm5z44vtUFHx4-v76GPHyuPR-WZGh7FXAt4LEOr4VkCjqq6t2yOAdwCr3xbbE10rqxMFX1-U-g-yy_ZT-l4g1TRih-0KmNUNKLXHni5HEwkTWZ6nfhrCtyHMKU4DRu6IbI_mBy-Ayf7B50fuE8eUgvGYS-Snz3fc_51wfcMXMdipwGEsfZ7viKccaZHDr5BLaqysx56yNzxiPmTbDodELzfvAfvy8cPn84vq6ubT5fnZVWXkDHLlLCFJbDpnJKpuBgpkWxsJvesJFFEHTlrqWlcj9GChFiAtKkm2JeUaecDerueW6-4nSlnPfTI0DDhSmJJuRa1qJboCNmvQxJBSJKcX0c8xPmoBeqldr7TrpVMNoFfa9TL3erNg6udk_0utPRfgzQbAZHBwEUfj0z_upIG2nhXsdI1RsfHgKepkPI2GrI9ksrbBP3PJb95fopM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71262618</pqid></control><display><type>article</type><title>Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Thorup, Christian ; Ollerstam, Anna ; Persson, A.Erik G ; Torffvit, Ole</creator><creatorcontrib>Thorup, Christian ; Ollerstam, Anna ; Persson, A.Erik G ; Torffvit, Ole</creatorcontrib><description>The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm–Horsfall protein (THP) secretion. Three groups of male Sprague–Dawley rats were studied: (A) diabetic rats with blood glucose levels (BG)<19 mmol/l, (B) with BG≥19 mmol/l, and (C) control rats. After 50 days, the diabetic rats had higher arterial blood pressure and increased TGF reactivity (Δ
P
SF) than control rats. The proximal tubular free-flow pressure (
P
T) and stop-flow pressure (
P
SF) were reduced, while the glomerular filtration was normal. This indicates that the diabetic animals of this study were severely vasoconstricted. Inhibition of renal nitric oxide synthase (NOS) resulted in a greater increase of TGF reactivity in diabetic rats than in control rats. Diabetic rats also showed increased excretion rates of albumin and THP. The excretion rate of THP was associated with
P
SF (
r=−0.88,
p<0.01). In conclusion, diabetes mellitus was associated with an increased blood pressure and an increased TGF reactivity, which indicates that the diabetic rats were vasoconstricted. NOS inhibition increased the reactivity of TGF to greater extent in diabetic animals than in controls, indicating that the renal vasoconstriction was compensated for by an increased NO production.</description><identifier>ISSN: 1056-8727</identifier><identifier>EISSN: 1873-460X</identifier><identifier>DOI: 10.1016/S1056-8727(00)00056-8</identifier><identifier>PMID: 10925066</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Associated diseases and complications ; Biological and medical sciences ; Blood Pressure ; Diabetes Mellitus, Experimental - physiopathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Enzyme Inhibitors - pharmacology ; Feedback ; Glomerular Filtration Rate ; Kidney Glomerulus - physiopathology ; Kidney Tubules - physiopathology ; Male ; Medical sciences ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - antagonists & inhibitors ; NO synthase ; Rats ; Rats, Sprague-Dawley ; Stop-flow pressure ; Tamm–Horsfall protein ; Tubuloglomerular feedback ; Vasoconstriction</subject><ispartof>Journal of diabetes and its complications, 2000, Vol.14 (1), p.46-52</ispartof><rights>2000 Elsevier Science Inc.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-fdeae3a58fc3a689060372c30bfbe06ee80f3de87f2a0b0d02103da63ed7e6f53</citedby><cites>FETCH-LOGICAL-c390t-fdeae3a58fc3a689060372c30bfbe06ee80f3de87f2a0b0d02103da63ed7e6f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1056872700000568$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27902,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1450729$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10925066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thorup, Christian</creatorcontrib><creatorcontrib>Ollerstam, Anna</creatorcontrib><creatorcontrib>Persson, A.Erik G</creatorcontrib><creatorcontrib>Torffvit, Ole</creatorcontrib><title>Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat</title><title>Journal of diabetes and its complications</title><addtitle>J Diabetes Complications</addtitle><description>The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm–Horsfall protein (THP) secretion. Three groups of male Sprague–Dawley rats were studied: (A) diabetic rats with blood glucose levels (BG)<19 mmol/l, (B) with BG≥19 mmol/l, and (C) control rats. After 50 days, the diabetic rats had higher arterial blood pressure and increased TGF reactivity (Δ
P
SF) than control rats. The proximal tubular free-flow pressure (
P
T) and stop-flow pressure (
P
SF) were reduced, while the glomerular filtration was normal. This indicates that the diabetic animals of this study were severely vasoconstricted. Inhibition of renal nitric oxide synthase (NOS) resulted in a greater increase of TGF reactivity in diabetic rats than in control rats. Diabetic rats also showed increased excretion rates of albumin and THP. The excretion rate of THP was associated with
P
SF (
r=−0.88,
p<0.01). In conclusion, diabetes mellitus was associated with an increased blood pressure and an increased TGF reactivity, which indicates that the diabetic rats were vasoconstricted. NOS inhibition increased the reactivity of TGF to greater extent in diabetic animals than in controls, indicating that the renal vasoconstriction was compensated for by an increased NO production.</description><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Feedback</subject><subject>Glomerular Filtration Rate</subject><subject>Kidney Glomerulus - physiopathology</subject><subject>Kidney Tubules - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>NO synthase</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Stop-flow pressure</subject><subject>Tamm–Horsfall protein</subject><subject>Tubuloglomerular feedback</subject><subject>Vasoconstriction</subject><issn>1056-8727</issn><issn>1873-460X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtP3TAQRi1UxLM_oZUXVUUXKeOYOLkrhFBbkBAsaKXurIk9Lm5z44vtUFHx4-v76GPHyuPR-WZGh7FXAt4LEOr4VkCjqq6t2yOAdwCr3xbbE10rqxMFX1-U-g-yy_ZT-l4g1TRih-0KmNUNKLXHni5HEwkTWZ6nfhrCtyHMKU4DRu6IbI_mBy-Ayf7B50fuE8eUgvGYS-Snz3fc_51wfcMXMdipwGEsfZ7viKccaZHDr5BLaqysx56yNzxiPmTbDodELzfvAfvy8cPn84vq6ubT5fnZVWXkDHLlLCFJbDpnJKpuBgpkWxsJvesJFFEHTlrqWlcj9GChFiAtKkm2JeUaecDerueW6-4nSlnPfTI0DDhSmJJuRa1qJboCNmvQxJBSJKcX0c8xPmoBeqldr7TrpVMNoFfa9TL3erNg6udk_0utPRfgzQbAZHBwEUfj0z_upIG2nhXsdI1RsfHgKepkPI2GrI9ksrbBP3PJb95fopM</recordid><startdate>2000</startdate><enddate>2000</enddate><creator>Thorup, Christian</creator><creator>Ollerstam, Anna</creator><creator>Persson, A.Erik G</creator><creator>Torffvit, Ole</creator><general>Elsevier Inc</general><general>Elsevier Science</general><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>7X8</scope></search><sort><creationdate>2000</creationdate><title>Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat</title><author>Thorup, Christian ; Ollerstam, Anna ; Persson, A.Erik G ; Torffvit, Ole</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-fdeae3a58fc3a689060372c30bfbe06ee80f3de87f2a0b0d02103da63ed7e6f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Feedback</topic><topic>Glomerular Filtration Rate</topic><topic>Kidney Glomerulus - physiopathology</topic><topic>Kidney Tubules - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>NO synthase</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Stop-flow pressure</topic><topic>Tamm–Horsfall protein</topic><topic>Tubuloglomerular feedback</topic><topic>Vasoconstriction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thorup, Christian</creatorcontrib><creatorcontrib>Ollerstam, Anna</creatorcontrib><creatorcontrib>Persson, A.Erik G</creatorcontrib><creatorcontrib>Torffvit, Ole</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Journal of diabetes and its complications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thorup, Christian</au><au>Ollerstam, Anna</au><au>Persson, A.Erik G</au><au>Torffvit, Ole</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat</atitle><jtitle>Journal of diabetes and its complications</jtitle><addtitle>J Diabetes Complications</addtitle><date>2000</date><risdate>2000</risdate><volume>14</volume><issue>1</issue><spage>46</spage><epage>52</epage><pages>46-52</pages><issn>1056-8727</issn><eissn>1873-460X</eissn><abstract>The characteristics of the tubuloglomerular feedback (TGF) mechanism were examined in streptozotocin-diabetic rats. This model is known to induce damage in the distal tubular system and thus Tamm–Horsfall protein (THP) secretion. Three groups of male Sprague–Dawley rats were studied: (A) diabetic rats with blood glucose levels (BG)<19 mmol/l, (B) with BG≥19 mmol/l, and (C) control rats. After 50 days, the diabetic rats had higher arterial blood pressure and increased TGF reactivity (Δ
P
SF) than control rats. The proximal tubular free-flow pressure (
P
T) and stop-flow pressure (
P
SF) were reduced, while the glomerular filtration was normal. This indicates that the diabetic animals of this study were severely vasoconstricted. Inhibition of renal nitric oxide synthase (NOS) resulted in a greater increase of TGF reactivity in diabetic rats than in control rats. Diabetic rats also showed increased excretion rates of albumin and THP. The excretion rate of THP was associated with
P
SF (
r=−0.88,
p<0.01). In conclusion, diabetes mellitus was associated with an increased blood pressure and an increased TGF reactivity, which indicates that the diabetic rats were vasoconstricted. NOS inhibition increased the reactivity of TGF to greater extent in diabetic animals than in controls, indicating that the renal vasoconstriction was compensated for by an increased NO production.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10925066</pmid><doi>10.1016/S1056-8727(00)00056-8</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Associated diseases and complications Biological and medical sciences Blood Pressure Diabetes Mellitus, Experimental - physiopathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Enzyme Inhibitors - pharmacology Feedback Glomerular Filtration Rate Kidney Glomerulus - physiopathology Kidney Tubules - physiopathology Male Medical sciences NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - biosynthesis Nitric Oxide Synthase - antagonists & inhibitors NO synthase Rats Rats, Sprague-Dawley Stop-flow pressure Tamm–Horsfall protein Tubuloglomerular feedback Vasoconstriction |
| title | Increased tubuloglomerular feedback reactivity is associated with increased NO production in the streptozotocin-diabetic rat |
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