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Article ; Online: Adenosine reuptake inhibition reduces diabetes-induced glomerular hyperfiltration via the adenosine A2

Persson, Patrik / Fasching, Angelica / Pihl, Liselotte / Palm, Fredrik

American journal of physiology. Regulatory, integrative and comparative physiology

2023 Volume 325, Issue 4, Page(s) R337–R343

Abstract: Diabetes-induced glomerular hyperfiltration is an early alteration in kidney function in diabetes. Previous studies have shown that reduced adenosine ... ...

Abstract	Diabetes-induced glomerular hyperfiltration is an early alteration in kidney function in diabetes. Previous studies have shown that reduced adenosine A2
MeSH term(s)	Rats ; Animals ; Male ; Rats, Sprague-Dawley ; Dilazep/pharmacology ; Adenosine/pharmacology ; Kidney Glomerulus ; Diabetes Mellitus ; Kidney ; Kidney Diseases ; Glomerular Filtration Rate
Chemical Substances	Dilazep (F8KLC2BD5Z) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2023-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00278.2022
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Article ; Online: Acute intrarenal angiotensin (1-7) infusion decreases diabetes-induced glomerular hyperfiltration but increases kidney oxygen consumption in the rat.

Persson, Patrik / Fasching, Angelica / Palm, Fredrik

Acta physiologica (Oxford, England)

2019 Volume 226, Issue 1, Page(s) e13254

Abstract: Aim: Common kidney alterations early after the onset of insulinopenic diabetes include glomerular hyperfiltration, increased oxygen consumption and tissue hypoxia. Increased activity of the renin-angiotensin-aldosterone system (RAAS) has been implicated ...

Abstract	Aim: Common kidney alterations early after the onset of insulinopenic diabetes include glomerular hyperfiltration, increased oxygen consumption and tissue hypoxia. Increased activity of the renin-angiotensin-aldosterone system (RAAS) has been implicated in most of these early alterations. The RAAS peptide angiotensin (1-7) has the potential to modulate RAAS-mediated alterations in kidney function. Thus, the aim of the present study was to determine the acute effects of angiotensin (1-7) in the kidney of insulinopenic type 1 diabetic rat and the results compared to that of normoglycaemic controls. Methods: Renal haemodynamics and oxygen homeostasis were measured 3 weeks after administration of streptozotocin before and after acute intrarenal infusion of angiotensin (1-7) at a dose of 400 ng min Results: Arterial pressure and renal blood flow were similar between groups and not affected by exogenous angiotensin (1-7). Diabetics presented with glomerular hyperfiltration, increased urinary sodium excretion and elevated kidney oxygen consumption. Angiotensin (1-7) infusion normalized glomerular filtration, increased urinary sodium excretion, decreased proximal tubular reabsorption, and elevated kidney oxygen consumption even further. The latter resulting in tubular electrolyte transport inefficiency. Angiotensin (1-7) did not affect tissue oxygen tension and had no significant effects in controls on any of the measured parameters. Conclusion: Diabetes results in increased responsiveness to elevated levels of angiotensin (1-7) which is manifested as inhibition of tubular sodium transport and normalization of glomerular filtration. Furthermore, elevated angiotensin (1-7) levels increase kidney oxygen consumption in the diabetic kidney even further which affects tubular electrolyte transport efficiency negatively.
MeSH term(s)	Angiotensin I/pharmacology ; Animals ; Diabetes Mellitus, Experimental/complications ; Diabetic Nephropathies/drug therapy ; Kidney/metabolism ; Male ; Oxygen Consumption/drug effects ; Peptide Fragments/pharmacology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Peptide Fragments ; Angiotensin I (9041-90-1) ; angiotensin I (1-7) (IJ3FUK8MOF)
Language	English
Publishing date	2019-02-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13254
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Article ; Online: Intrarenal activation of endothelin type B receptors improves kidney oxygenation in type 1 diabetic rats.

Franzén, Stephanie / Pihl, Liselotte / Fasching, Angelica / Palm, Fredrik

American journal of physiology. Renal physiology

2017 Volume 314, Issue 3, Page(s) F439–F444

Abstract: About one-third of patients with type 1 diabetes develops kidney disease. The mechanism is largely unknown, but intrarenal hypoxia has been proposed as a unifying mechanism for chronic kidney disease, including diabetic nephropathy. The endothelin system ...

Abstract	About one-third of patients with type 1 diabetes develops kidney disease. The mechanism is largely unknown, but intrarenal hypoxia has been proposed as a unifying mechanism for chronic kidney disease, including diabetic nephropathy. The endothelin system has recently been demonstrated to regulate oxygen availability in the diabetic kidney via a pathway involving endothelin type A receptors (ETA-R). These receptors mainly mediate vasoconstriction and tubular sodium retention, and inhibition of ETA-R improves intrarenal oxygenation in the diabetic kidney. Endothelin type B receptors (ETB-R) can induce vasodilation of the renal vasculature and also regulate tubular sodium handling. However, the role of ETB-R in kidney oxygen homeostasis is unknown. The effects of acute intrarenal ETB-R activation (sarafotoxin 6c for 30-40 min; 0.78 pmol/h directly into the renal artery) on kidney function and oxygen metabolism were investigated in normoglycemic controls and insulinopenic male Sprague-Dawley rats administered streptozotocin (55 mg/kg) 2 wk before the acute experiments. Intrarenal activation of ETB-R improved oxygenation in the hypoxic diabetic kidney. However, the effects on diabetes-induced increased kidney oxygen consumption could not explain the improved oxygenation. Rather, the improved kidney oxygenation was due to hemodynamic effects increasing oxygen delivery without increasing glomerular filtration or tubular sodium load. In conclusion, increased ETB-R signaling in the diabetic kidney improves intrarenal tissue oxygenation due to increased oxygen delivery secondary to increased renal blood flow.
MeSH term(s)	Animals ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/physiopathology ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/chemically induced ; Diabetes Mellitus, Type 1/drug therapy ; Diabetes Mellitus, Type 1/physiopathology ; Diabetic Nephropathies/blood ; Diabetic Nephropathies/chemically induced ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/physiopathology ; Hemodynamics/drug effects ; Kidney/drug effects ; Kidney/metabolism ; Kidney/physiopathology ; Male ; Oxygen/blood ; Rats, Sprague-Dawley ; Receptor, Endothelin B/agonists ; Receptor, Endothelin B/metabolism ; Renal Circulation/drug effects ; Signal Transduction/drug effects ; Streptozocin ; Viper Venoms/pharmacology
Chemical Substances	Receptor, Endothelin B ; Viper Venoms ; ednrb protein, rat ; sarafotoxins s6 ; Streptozocin (5W494URQ81) ; Oxygen (S88TT14065)
Language	English
Publishing date	2017-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00498.2017
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Article ; Online: Pharmacological HIF-PHD inhibition reduces renovascular resistance and increases glomerular filtration by stimulating nitric oxide generation.

Burmakin, Mikhail / Fasching, Angelica / Kobayashi, Hanako / Urrutia, Andrés A / Damdimopoulos, Anastasios / Palm, Fredrik / Haase, Volker H

Acta physiologica (Oxford, England)

2021 Volume 233, Issue 1, Page(s) e13668

Abstract: Aim: Hypoxia-inducible factors (HIFs) are O: Methods: Using a cross-sectional study design, we investigated renal haemodynamics, O: Results: Systemic administration of roxadustat or molidustat resulted in a dose-dependent reduction in renovascular ...

Abstract	Aim: Hypoxia-inducible factors (HIFs) are O Methods: Using a cross-sectional study design, we investigated renal haemodynamics, O Results: Systemic administration of roxadustat or molidustat resulted in a dose-dependent reduction in renovascular resistance (RVR). This was associated with increased glomerular filtration rate (GFR), urine flow and tubular sodium transport rate (T Conclusions: Our data provide mechanistic insights into dose-dependent effects of short-term pharmacological HIF activation on renal haemodynamics, glomerular filtration and O
MeSH term(s)	Animals ; Biological Phenomena ; Cross-Sectional Studies ; Hypoxia-Inducible Factor-Proline Dioxygenases ; Nitric Oxide ; Prolyl Hydroxylases ; Rats ; Renal Insufficiency, Chronic
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Prolyl Hydroxylases (EC 1.14.11.-) ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29)
Language	English
Publishing date	2021-05-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13668
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Article ; Online: Iodinated contrast media inhibit oxygen consumption in freshly isolated proximal tubular cells from elderly humans and diabetic rats: Influence of nitric oxide.

Liss, Per / Hansell, Peter / Fasching, Angelica / Palm, Fredrik

Upsala journal of medical sciences

2016 Volume 121, Issue 1, Page(s) 12–16

Abstract: Objectives Mechanisms underlying contrast medium (CM)-induced nephropathy remain elusive, but recent attention has been directed to oxygen availability. The purpose of this study was to evaluate the effect of the low-osmolar CM iopromide and the iso- ... ...

Abstract	Objectives Mechanisms underlying contrast medium (CM)-induced nephropathy remain elusive, but recent attention has been directed to oxygen availability. The purpose of this study was to evaluate the effect of the low-osmolar CM iopromide and the iso-osmolar CM iodixanol on oxygen consumption (QO2) in freshly isolated proximal tubular cells (PTC) from kidneys ablated from elderly humans undergoing nephrectomy for renal carcinomas and from normoglycemic or streptozotocin-diabetic rats. Materials PTC were isolated from human kidneys, or kidneys of normoglycemic or streptozotocin-diabetic rats. QO2 was measured with Clark-type microelectrodes in a gas-tight chamber with and without each CM (10 mg I/mL medium). L-NAME was used to inhibit nitric oxide (NO) production caused by nitric oxide synthase. Results Both CM reduced QO2 in human PTC (about -35%) which was prevented by L-NAME. PTC from normoglycemic rats were unaffected by iopromide, whereas iodixanol decreased QO2 (-34%). Both CM decreased QO2 in PTC from diabetic rats (-38% and -36%, respectively). L-NAME only prevented the effect of iopromide in the diabetic rat PTC. Conclusions These observations demonstrate that CM can induce NO release from isolated PTC in vitro, which affects QO2. Our results suggest that the induction of NO release and subsequent effect on the cellular oxygen metabolism are dependent on several factors, including CM type and pre-existing risk factors for the development of CM-induced nephropathy.
MeSH term(s)	Aged ; Animals ; Contrast Media/toxicity ; Diabetes Mellitus, Experimental/metabolism ; Humans ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Male ; Middle Aged ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/physiology ; Oxygen Consumption/drug effects ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Contrast Media ; Nitric Oxide (31C4KY9ESH) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	183949-4
ISSN	2000-1967 ; 0300-9734
ISSN (online)	2000-1967
ISSN	0300-9734
DOI	10.3109/03009734.2016.1144664
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Article ; Online: Cellular transport of l-arginine determines renal medullary blood flow in control rats, but not in diabetic rats despite enhanced cellular uptake capacity.

Persson, Patrik / Fasching, Angelica / Teerlink, Tom / Hansell, Peter / Palm, Fredrik

American journal of physiology. Renal physiology

2017 Volume 312, Issue 2, Page(s) F278–F283

Abstract: Diabetes mellitus is associated with decreased nitric oxide bioavailability thereby affecting renal blood flow regulation. Previous reports have demonstrated that cellular uptake of l-arginine is rate limiting for nitric oxide production and that plasma ... ...

Abstract	Diabetes mellitus is associated with decreased nitric oxide bioavailability thereby affecting renal blood flow regulation. Previous reports have demonstrated that cellular uptake of l-arginine is rate limiting for nitric oxide production and that plasma l-arginine concentration is decreased in diabetes. We therefore investigated whether regional renal blood flow regulation is affected by cellular l-arginine uptake in streptozotocin-induced diabetic rats. Rats were anesthetized with thiobutabarbital, and the left kidney was exposed. Total, cortical, and medullary renal blood flow was investigated before and after renal artery infusion of increasing doses of either l-homoarginine to inhibit cellular uptake of l-arginine or N
MeSH term(s)	Animals ; Arginine/metabolism ; Biological Transport/drug effects ; Diabetes Mellitus, Experimental/metabolism ; Enzyme Inhibitors/pharmacology ; Homoarginine/pharmacology ; Kidney Medulla/blood supply ; Kidney Medulla/drug effects ; Kidney Medulla/metabolism ; Male ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Renal Circulation/drug effects ; Renal Circulation/physiology
Chemical Substances	Enzyme Inhibitors ; Homoarginine (156-86-5) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2017-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00335.2016
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Article ; Online: Determinants of renal oxygen metabolism during low Na

Patinha, Daniela / Carvalho, Carla / Persson, Patrik / Pihl, Liselotte / Fasching, Angelica / Friederich-Persson, Malou / O'Neill, Julie / Palm, Fredrik

The Journal of physiology

2020 Volume 598, Issue 23, Page(s) 5573–5587

Abstract: Key points: Reducing Na: Abstract: Reduced ... ...

Abstract	Key points: Reducing Na Abstract: Reduced Na
MeSH term(s)	Aldosterone/metabolism ; Angiotensin II/metabolism ; Animals ; Blood Pressure ; Diet ; Kidney/metabolism ; Male ; Oxygen/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1/metabolism ; Receptors, Mineralocorticoid ; Renin-Angiotensin System
Chemical Substances	Receptor, Angiotensin, Type 1 ; Receptors, Mineralocorticoid ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Oxygen (S88TT14065)
Language	English
Publishing date	2020-09-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP280481
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Article ; Online: L-Citrulline, but not L-arginine, prevents diabetes mellitus-induced glomerular hyperfiltration and proteinuria in rat.

Persson, Patrik / Fasching, Angelica / Teerlink, Tom / Hansell, Peter / Palm, Fredrik

Hypertension (Dallas, Tex. : 1979)

2014 Volume 64, Issue 2, Page(s) 323–329

Abstract: Diabetes mellitus–induced oxidative stress causes increased renal oxygen consumption and intrarenal tissue hypoxia. Nitric oxide is an important determinant of renal oxygen consumption and electrolyte transport efficiency. The present study investigates ... ...

Abstract	Diabetes mellitus–induced oxidative stress causes increased renal oxygen consumption and intrarenal tissue hypoxia. Nitric oxide is an important determinant of renal oxygen consumption and electrolyte transport efficiency. The present study investigates whether l-arginine or l-citrulline to promote nitric oxide production prevents the diabetes mellitus–induced kidney dysfunction. Glomerular filtration rate, renal blood flow, in vivo oxygen consumption, tissue oxygen tension, and proteinuria were investigated in control and streptozotocin-diabetic rats with and without chronic l-arginine or l-citrulline treatment for 3 weeks. Untreated and l-arginine–treated diabetic rats displayed increased glomerular filtration rate (2600±162 versus 1599±127 and 2290±171 versus 1739±138 μL/min per kidney), whereas l-citrulline prevented the increase (1227±126 versus 1375±88 μL/min per kidney). Filtration fraction was increased in untreated diabetic rats because of the increase in glomerular filtration rate but not in l-arginine– or l-citrulline–treated diabetic rats. Urinary protein excretion was increased in untreated and l-arginine–treated diabetic rats (142±25 versus 75±7 and 128±7 versus 89±7 μg/min per kidney) but not in diabetic rats administered l-citrulline (67±7 versus 61±5 μg/min per kidney). The diabetes mellitus–induced tissue hypoxia, because of elevated oxygen consumption, was unaltered by any of the treatments. l-citrulline administered to diabetic rats increases plasma l-arginine concentration, which prevents the diabetes mellitus–induced glomerular hyperfiltration, filtration fraction, and proteinuria, possibly by a vascular effect.
MeSH term(s)	Animals ; Arginine/pharmacology ; Arginine/therapeutic use ; Citrulline/pharmacology ; Citrulline/therapeutic use ; Diabetes Mellitus, Experimental/physiopathology ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/physiopathology ; Diabetic Nephropathies/prevention & control ; Glomerular Filtration Rate/drug effects ; Glomerular Filtration Rate/physiology ; Kidney/drug effects ; Kidney/physiopathology ; Kidney Glomerulus/drug effects ; Kidney Glomerulus/physiopathology ; Oxygen Consumption/drug effects ; Proteinuria/drug therapy ; Proteinuria/physiopathology ; Proteinuria/prevention & control ; Rats
Chemical Substances	Citrulline (29VT07BGDA) ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2014-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.114.03519
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Article: Hypoxia in the diabetic kidney is independent of advanced glycation end-products.

Nordquist, Lina / Liss, Per / Fasching, Angelica / Hansell, Peter / Palm, Fredrik

Advances in experimental medicine and biology

2013 Volume 765, Page(s) 185–193

Abstract: Sustained hyperglycemia is closely associated with increased risk to develop nephropathy. We have previously reported alterations in the intrarenal oxygen metabolism already after the early onset of diabetes. Furthermore, formation of advanced glycation ... ...

Abstract	Sustained hyperglycemia is closely associated with increased risk to develop nephropathy. We have previously reported alterations in the intrarenal oxygen metabolism already after the early onset of diabetes. Furthermore, formation of advanced glycation end-products (AGE) is postulated as a major contributor to diabetic nephropathy. We therefore investigated the possible relationship between altered oxygen metabolism and AGE in diabetic kidneys.Normoglycemic and streptozotocin-diabetic rats with and without chronic treatment with aminoguanidine (AGE inhibitor; 600 mg/kg bw/24 h in drinking water) or L-N(6)-(1-Iminoethyl)lysine (L-NIL, iNOS inhibitor, 1 mg/kg bw/24 h in drinking water) were studied 2 weeks after induction of diabetes. Glomerular filtration rate (GFR) was estimated by inulin clearance, oxygen tension (pO(2)) and interstitial pH by microelectrodes and regional renal blood flow (RBF) by laser-Doppler. Histological changes were evaluated on fixed tissue.Glomerular hyperfiltration was unaffected by aminoguanidine, whereas L-NIL normalized GFR in diabetic rats. pO(2) and interstitial pH, but not RBF, were lower in both kidney cortex and medulla compared to control rats, but was unaffected by both chronic treatments. Urinary protein excretion was higher in diabetic rats and unaffected by L-NIL, whereas aminoguanidine paradoxically increased this parameter. Damage scores were similar in all groups.In conclusion, diabetes-induced alterations in intrarenal oxygen metabolism are independent of the AGE pathway, and precede any morphological changes. These findings highlight the early stage of diabetes as being a metabolic disorder also in the kidney.
MeSH term(s)	Animals ; Diabetes Complications/drug therapy ; Diabetes Complications/etiology ; Diabetes Complications/metabolism ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Enzyme Inhibitors/therapeutic use ; Glomerular Filtration Rate ; Glycation End Products, Advanced/metabolism ; Guanidines/therapeutic use ; Hypoxia/metabolism ; Hypoxia/pathology ; Kidney/metabolism ; Kidney/pathology ; Kidney Function Tests ; Male ; Nitric Oxide Synthase/antagonists & inhibitors ; Rats ; Rats, Inbred WF
Chemical Substances	Enzyme Inhibitors ; Glycation End Products, Advanced ; Guanidines ; Nitric Oxide Synthase (EC 1.14.13.39) ; pimagedine (SCQ4EZQ113)
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-1-4614-4989-8_26
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Article ; Online: Acute SGLT inhibition normalizes O2 tension in the renal cortex but causes hypoxia in the renal medulla in anaesthetized control and diabetic rats.

O'Neill, Julie / Fasching, Angelica / Pihl, Liselotte / Patinha, Daniela / Franzén, Stephanie / Palm, Fredrik

American journal of physiology. Renal physiology

2015 Volume 309, Issue 3, Page(s) F227–34

Abstract: Early stage diabetic nephropathy is characterized by glomerular hyperfiltration and reduced renal tissue Po2. Recent observations have indicated that increased tubular Na(+)-glucose linked transport (SGLT) plays a role in the development of diabetes- ... ...

Abstract	Early stage diabetic nephropathy is characterized by glomerular hyperfiltration and reduced renal tissue Po2. Recent observations have indicated that increased tubular Na(+)-glucose linked transport (SGLT) plays a role in the development of diabetes-induced hyperfiltration. The aim of the present study was to determine how inhibition of SLGT impacts upon Po2 in the diabetic rat kidney. Diabetes was induced by streptozotocin in Sprague-Dawley rats 2 wk before experimentation. Renal hemodynamics, excretory function, and renal O2 homeostasis were measured in anesthetized control and diabetic rats during baseline and after acute SGLT inhibition using phlorizin (200 mg/kg ip). Baseline arterial pressure was similar in both groups and unaffected by SGLT inhibition. Diabetic animals displayed reduced baseline Po2 in both the cortex and medulla. SGLT inhibition improved cortical Po2 in the diabetic kidney, whereas it reduced medullary Po2 in both groups. SGLT inhibition reduced Na(+) transport efficiency [tubular Na(+) transport (TNa)/renal O2 consumption (Qo2)] in the control kidney, whereas the already reduced TNa/Qo2 in the diabetic kidney was unaffected by SGLT inhibition. In conclusion, these data demonstrate that when SGLT is inhibited, renal cortex Po2 in the diabetic rat kidney is normalized, which implies that increased proximal tubule transport contributes to the development of hypoxia in the diabetic kidney. The reduction in medullary Po2 in both control and diabetic kidneys during the inhibition of proximal Na(+) reabsorption suggests the redistribution of active Na(+) transport to less efficient nephron segments, such as the medullary thick ascending limb, which results in medullary hypoxia.
MeSH term(s)	Anesthesia ; Animals ; Arterial Pressure/drug effects ; Diabetes Mellitus, Experimental ; Diabetic Nephropathies/metabolism ; Hypoxia/metabolism ; Kidney Cortex/drug effects ; Kidney Cortex/metabolism ; Kidney Medulla/metabolism ; Male ; Oxygen Consumption/drug effects ; Phlorhizin/pharmacology ; Rats ; Rats, Sprague-Dawley ; Sodium/metabolism ; Sodium-Glucose Transport Proteins/antagonists & inhibitors ; Urodynamics/drug effects
Chemical Substances	Sodium-Glucose Transport Proteins ; Sodium (9NEZ333N27) ; Phlorhizin (CU9S17279X)
Language	English
Publishing date	2015-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00689.2014
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