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Exercise training protects the renal circulation against high glucose challenge

It has been shown previously that high glucose causes direct and acute endothelial dysfunction in non‐diabetic isolated rabbit kidney. This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined...

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Published in:Fundamental & clinical pharmacology 2005-10, Vol.19 (5), p.537-543
Main Authors: De Moraes, Roger, Gioseffi, Giovanni, Lopes, Nuno do Nascimento, Gomes, Marilia Brito, Nóbrega, Antonio Claudio Lucas, Tibiriçá, Eduardo
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container_title Fundamental & clinical pharmacology
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description It has been shown previously that high glucose causes direct and acute endothelial dysfunction in non‐diabetic isolated rabbit kidney. This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12‐week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs–Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d‐glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose‐related vasodilator responses, reaching the maximum of 41 ± 2% (n = 10; P 
doi_str_mv 10.1111/j.1472-8206.2005.00358.x
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This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12‐week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs–Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d‐glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose‐related vasodilator responses, reaching the maximum of 41 ± 2% (n = 10; P &lt; 0.05). In the kidneys perfused with high concentrations of glucose (SED 15), endothelium‐dependent vasodilation was significantly blunted. Maximal relaxation in the presence of 15 mm glucose was of 19 ± 2%, which was significantly different from the SED 5.5 group (41 ± 2%, n = 10, P &lt; 0.01). In the ExT 5.5 group, ACh‐induced vasodilation was significantly enhanced when compared with the SED 5.5 group, reaching the maximum of (52 ± 2%, n = 10, P &lt; 0.05). Moreover, the exposure of the renal circulation of ExT animals to high glucose did not change endothelium‐dependent vasodilation induced by ACh (46 ± 3%, n = 6), when compared with the ExT 5.5 group. Finally, exercise training prevented the deleterious effects of high glucose on endothelial‐dependent renal vasodilation (SED 15: 19 ± 2% vs. ExT 15: 46 ± 3%; P &lt; 0.05). It is concluded that exercise training protects the rabbit renal circulation against endothelial dysfunction elicited by acute exposure to moderately elevated glucose levels, corresponding to the postprandial glycemia of diabetes type 2 patients under treatment. 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This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12‐week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs–Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d‐glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose‐related vasodilator responses, reaching the maximum of 41 ± 2% (n = 10; P &lt; 0.05). In the kidneys perfused with high concentrations of glucose (SED 15), endothelium‐dependent vasodilation was significantly blunted. Maximal relaxation in the presence of 15 mm glucose was of 19 ± 2%, which was significantly different from the SED 5.5 group (41 ± 2%, n = 10, P &lt; 0.01). In the ExT 5.5 group, ACh‐induced vasodilation was significantly enhanced when compared with the SED 5.5 group, reaching the maximum of (52 ± 2%, n = 10, P &lt; 0.05). Moreover, the exposure of the renal circulation of ExT animals to high glucose did not change endothelium‐dependent vasodilation induced by ACh (46 ± 3%, n = 6), when compared with the ExT 5.5 group. Finally, exercise training prevented the deleterious effects of high glucose on endothelial‐dependent renal vasodilation (SED 15: 19 ± 2% vs. ExT 15: 46 ± 3%; P &lt; 0.05). It is concluded that exercise training protects the rabbit renal circulation against endothelial dysfunction elicited by acute exposure to moderately elevated glucose levels, corresponding to the postprandial glycemia of diabetes type 2 patients under treatment. 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Impaired glucose tolerance</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelium, Vascular - physiology</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Exercise Test - methods</topic><topic>Female</topic><topic>Glucose - administration &amp; dosage</topic><topic>Glucose - pharmacology</topic><topic>hyperglycemia</topic><topic>In Vitro Techniques</topic><topic>Injections, Intravenous</topic><topic>isolated rabbit kidney</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Pharmacology. 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This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12‐week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs–Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d‐glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose‐related vasodilator responses, reaching the maximum of 41 ± 2% (n = 10; P &lt; 0.05). In the kidneys perfused with high concentrations of glucose (SED 15), endothelium‐dependent vasodilation was significantly blunted. Maximal relaxation in the presence of 15 mm glucose was of 19 ± 2%, which was significantly different from the SED 5.5 group (41 ± 2%, n = 10, P &lt; 0.01). In the ExT 5.5 group, ACh‐induced vasodilation was significantly enhanced when compared with the SED 5.5 group, reaching the maximum of (52 ± 2%, n = 10, P &lt; 0.05). Moreover, the exposure of the renal circulation of ExT animals to high glucose did not change endothelium‐dependent vasodilation induced by ACh (46 ± 3%, n = 6), when compared with the ExT 5.5 group. Finally, exercise training prevented the deleterious effects of high glucose on endothelial‐dependent renal vasodilation (SED 15: 19 ± 2% vs. ExT 15: 46 ± 3%; P &lt; 0.05). It is concluded that exercise training protects the rabbit renal circulation against endothelial dysfunction elicited by acute exposure to moderately elevated glucose levels, corresponding to the postprandial glycemia of diabetes type 2 patients under treatment. The enhanced renal vasodilator reserve elicited by exercise training turns out to be a response that protects the kidney from the deleterious effects of glycemic peaks.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>16176332</pmid><doi>10.1111/j.1472-8206.2005.00358.x</doi><tpages>7</tpages></addata></record>
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subjects Acetylcholine - pharmacology
Animals
Biological and medical sciences
diabetes mellitus
Diabetes. Impaired glucose tolerance
Dose-Response Relationship, Drug
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Endothelium, Vascular - physiology
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Exercise Test - methods
Female
Glucose - administration & dosage
Glucose - pharmacology
hyperglycemia
In Vitro Techniques
Injections, Intravenous
isolated rabbit kidney
Kidney - blood supply
Kidney - drug effects
Kidney - physiology
Male
Medical sciences
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - physiology
Pharmacology. Drug treatments
Physical Conditioning, Animal - methods
Physical Conditioning, Animal - physiology
Rabbits
Renal Circulation - drug effects
Renal Circulation - physiology
Time Factors
vascular reactivity
Vasodilation - drug effects
Vasodilator Agents - pharmacology
title Exercise training protects the renal circulation against high glucose challenge
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