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Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level
Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondia...
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| Published in: | Journal of physiology and pharmacology : an official journal of the Polish Physiological Society 2003-03, Vol.54 (1), p.109-120 |
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| container_title | Journal of physiology and pharmacology : an official journal of the Polish Physiological Society |
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| creator | Szczepańska-Konkel, M Jankowski, M Stiepanow-Trzeciak, A Rudzik, A Pawełczyk, T Angielski, S |
| description | Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondiabetic (ND)-rats. In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p < 0.05) and ND-rats (p < 0.02). Intravenous infusion of 5 nmol x min(-1) x kg(-1) NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 micromol x min(-1) x kg(-1) ) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group. compared with ND-group (p < 0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition. |
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In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p < 0.05) and ND-rats (p < 0.02). Intravenous infusion of 5 nmol x min(-1) x kg(-1) NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 micromol x min(-1) x kg(-1) ) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group. compared with ND-group (p < 0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition.</description><identifier>ISSN: 0867-5910</identifier><identifier>PMID: 12674223</identifier><language>eng</language><publisher>Poland</publisher><subject>Adenosine - physiology ; Animals ; Blood Glucose - physiology ; Diabetes Mellitus, Experimental - physiopathology ; Glomerular Filtration Rate - drug effects ; Hemodynamics - drug effects ; Hemodynamics - physiology ; Inulin ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - physiopathology ; Male ; NAD - pharmacology ; Purinergic P1 Receptor Antagonists ; Rats ; Rats, Wistar ; Renal Plasma Flow - drug effects ; Xanthines - pharmacology</subject><ispartof>Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 2003-03, Vol.54 (1), p.109-120</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12674223$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Szczepańska-Konkel, M</creatorcontrib><creatorcontrib>Jankowski, M</creatorcontrib><creatorcontrib>Stiepanow-Trzeciak, A</creatorcontrib><creatorcontrib>Rudzik, A</creatorcontrib><creatorcontrib>Pawełczyk, T</creatorcontrib><creatorcontrib>Angielski, S</creatorcontrib><title>Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level</title><title>Journal of physiology and pharmacology : an official journal of the Polish Physiological Society</title><addtitle>J Physiol Pharmacol</addtitle><description>Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondiabetic (ND)-rats. In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p < 0.05) and ND-rats (p < 0.02). Intravenous infusion of 5 nmol x min(-1) x kg(-1) NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 micromol x min(-1) x kg(-1) ) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group. compared with ND-group (p < 0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition.</description><subject>Adenosine - physiology</subject><subject>Animals</subject><subject>Blood Glucose - physiology</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Hemodynamics - physiology</subject><subject>Inulin</subject><subject>Kidney Glomerulus - drug effects</subject><subject>Kidney Glomerulus - physiopathology</subject><subject>Male</subject><subject>NAD - pharmacology</subject><subject>Purinergic P1 Receptor Antagonists</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal Plasma Flow - drug effects</subject><subject>Xanthines - pharmacology</subject><issn>0867-5910</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNo1kLtOwzAYRj2AaCm8AvLEFim-xE5GVHGTKiGh7pFj_ylGjm1sp6I8PZEo01nOd4bvAq3rVsiq6Ui9Qtc5f9Y1JZyJK7QiVEhOKVuj73fIMfhsj-AhZxxGnMArhw8uTJBmZ3EJWBnwIVsP2HqcS4JYwk8oQVtfWW9mDQYbqwYoVuOkSsYGIvhlVXDw-OMUIR3cSSuYrMIOjuBu0OWoXIbbMzdo__S4375Uu7fn1-3Droq0lqUyTImGARMNASGZWSiGVneccsq45o0amAHKjew6TfmwOGygjSRCjpwKtkH3f9mYwtcMufSTzRqcUx7CnHvJiKS8bRfx7izOwwSmj8lOKp36_6vYL7aNZmw</recordid><startdate>200303</startdate><enddate>200303</enddate><creator>Szczepańska-Konkel, M</creator><creator>Jankowski, M</creator><creator>Stiepanow-Trzeciak, A</creator><creator>Rudzik, A</creator><creator>Pawełczyk, T</creator><creator>Angielski, S</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200303</creationdate><title>Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level</title><author>Szczepańska-Konkel, M ; Jankowski, M ; Stiepanow-Trzeciak, A ; Rudzik, A ; Pawełczyk, T ; Angielski, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p207t-d3a653e3651e673d6516b8c9424234c45ab3de24d799c24b6733b257167f4263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adenosine - physiology</topic><topic>Animals</topic><topic>Blood Glucose - physiology</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Hemodynamics - physiology</topic><topic>Inulin</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - physiopathology</topic><topic>Male</topic><topic>NAD - pharmacology</topic><topic>Purinergic P1 Receptor Antagonists</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal Plasma Flow - drug effects</topic><topic>Xanthines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Szczepańska-Konkel, M</creatorcontrib><creatorcontrib>Jankowski, M</creatorcontrib><creatorcontrib>Stiepanow-Trzeciak, A</creatorcontrib><creatorcontrib>Rudzik, A</creatorcontrib><creatorcontrib>Pawełczyk, T</creatorcontrib><creatorcontrib>Angielski, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of physiology and pharmacology : an official journal of the Polish Physiological Society</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Szczepańska-Konkel, M</au><au>Jankowski, M</au><au>Stiepanow-Trzeciak, A</au><au>Rudzik, A</au><au>Pawełczyk, T</au><au>Angielski, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level</atitle><jtitle>Journal of physiology and pharmacology : an official journal of the Polish Physiological Society</jtitle><addtitle>J Physiol Pharmacol</addtitle><date>2003-03</date><risdate>2003</risdate><volume>54</volume><issue>1</issue><spage>109</spage><epage>120</epage><pages>109-120</pages><issn>0867-5910</issn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Glomerular filtration rate (GFR) in response to adenosine precursor, NAD, and glomeruli contractility in response to adenosine were evaluated in streptozotocin-induced diabetic rats with severe (blood glucose 27.8 +/- 1.2 mmol/L) and moderate hyperglycaemia (18.2 +/- 0.9 mmol/L) compared with nondiabetic (ND)-rats. In anaesthetised rats, basal GFR was greater in moderately diabetic rats compared with severely diabetic rats (p < 0.05) and ND-rats (p < 0.02). Intravenous infusion of 5 nmol x min(-1) x kg(-1) NAD reduced GFR and renal plasma flow (RPF) in diabetic rats but had no effect on these parameters in ND-rats. Moreover, NAD-induced reduction of GFR and RPF was greater in rats with severe diabetes (41% and 30%, respectively) than in with moderate diabetes (25% and 26%, respectively). Theophylline (0.2 micromol x min(-1) x kg(-1) ) abolished renal response to NAD. Isolated glomeruli contraction in response to adenosine, assessed by glomerular 3H-inulin space reduction, was lowered in moderately diabetic-group and enhanced in severely diabetic-group. compared with ND-group (p < 0.05). Adenosine A1-receptor antagonist DPCPX inhibited adenosine-induced glomeruli contraction. This differential response of diabetic renal glomeruli to adenosine suggests that impaired glomerular contractility in response to adenosine could be responsible for hyperfiltration in moderate diabets, whereas, the increased adenosine-dependent contractility of glomeruli in severe diabetes may increase the risk of acute renal failure in this condition.</abstract><cop>Poland</cop><pmid>12674223</pmid><tpages>12</tpages></addata></record> |
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| ispartof | Journal of physiology and pharmacology : an official journal of the Polish Physiological Society, 2003-03, Vol.54 (1), p.109-120 |
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| subjects | Adenosine - physiology Animals Blood Glucose - physiology Diabetes Mellitus, Experimental - physiopathology Glomerular Filtration Rate - drug effects Hemodynamics - drug effects Hemodynamics - physiology Inulin Kidney Glomerulus - drug effects Kidney Glomerulus - physiopathology Male NAD - pharmacology Purinergic P1 Receptor Antagonists Rats Rats, Wistar Renal Plasma Flow - drug effects Xanthines - pharmacology |
| title | Responsiveness of renal glomeruli to adenosine in streptozotocin-induced diabetic rats dependent on hyperglycaemia level |
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