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Role of connecting tubule glomerular feedback in obesity related renal damage

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Název: Role of connecting tubule glomerular feedback in obesity related renal damage
Autoři: Monu, Sumit R, Maheshwari, Mani, Peterson, Edward L, Carretero, Oscar A
Zdroj: Public Health Sciences Articles
Informace o vydavateli: Henry Ford Health Scholarly Commons
Rok vydání: 2018
Sbírka: Henry Ford Health System Scholarly Commons
Témata: Animals, Arterial Pressure, Connective Tissue Growth Factor/metabolism, Disease Models, Animal, Feedback, Physiological, Glomerular Filtration Rate, Kidney Diseases/etiology/metabolism/pathology/physiopathology, Kidney Glomerulus/blood supply/metabolism/pathology, Kidney Tubules/metabolism/pathology/physiopathology, Microcirculation, Obesity/complications, Proteinuria/etiology/metabolism/pathology/physiopathology, Rats, Zucker, Renal Circulation, Signal Transduction, Up-Regulation, Ctgf, Tgf, obesity, renal damage
Popis: Zucker obese rats (ZOR) have higher glomerular capillary pressure (PGC) that can cause renal damage. PGC is controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resistance is regulated by factors that regulate other arterioles, such as myogenic response. In addition, it is also regulated by 2 intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that increased CTGF contributes to TGF attenuation, which in turn increases PGC in ZOR. We performed a renal micropuncture experiment and measured stop-flow pressure (PSF), which is an indirect measurement of PGC in ZOR. Maximal TGF response at 40 nl/min was attenuated in ZOR (4.47 ± 0.60 mmHg) in comparison to the Zucker lean rats (ZLR; 8.54 ± 0.73 mmHg, P < 0.05), and CTGF was elevated in ZOR (5.34 ± 0.87 mmHg) compared with ZLR (1.12 ± 1.28 mmHg, P < 0.05). CTGF inhibition with epithelial sodium channel blocker normalized the maximum PSF change in ZOR indicating that CTGF plays a significant role in TGF attenuation (ZOR, 10.67 ± 1.07 mmHg vs. ZLR, 9.5 ± 1.53 mmHg). We conclude that enhanced CTGF contributes to TGF attenuation in ZOR and potentially contribute to progressive renal damage.
Druh dokumentu: text
Jazyk: unknown
Relation: https://scholarlycommons.henryford.com/publichealthsciences_articles/131; https://libkey.io/libraries/106/gotofulltext/pmid/30303713
Dostupnost: https://scholarlycommons.henryford.com/publichealthsciences_articles/131
https://libkey.io/libraries/106/gotofulltext/pmid/30303713
Přístupové číslo: edsbas.E95DF4DE
Databáze: BASE
Popis
Abstrakt:Zucker obese rats (ZOR) have higher glomerular capillary pressure (PGC) that can cause renal damage. PGC is controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resistance is regulated by factors that regulate other arterioles, such as myogenic response. In addition, it is also regulated by 2 intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that increased CTGF contributes to TGF attenuation, which in turn increases PGC in ZOR. We performed a renal micropuncture experiment and measured stop-flow pressure (PSF), which is an indirect measurement of PGC in ZOR. Maximal TGF response at 40 nl/min was attenuated in ZOR (4.47 ± 0.60 mmHg) in comparison to the Zucker lean rats (ZLR; 8.54 ± 0.73 mmHg, P < 0.05), and CTGF was elevated in ZOR (5.34 ± 0.87 mmHg) compared with ZLR (1.12 ± 1.28 mmHg, P < 0.05). CTGF inhibition with epithelial sodium channel blocker normalized the maximum PSF change in ZOR indicating that CTGF plays a significant role in TGF attenuation (ZOR, 10.67 ± 1.07 mmHg vs. ZLR, 9.5 ± 1.53 mmHg). We conclude that enhanced CTGF contributes to TGF attenuation in ZOR and potentially contribute to progressive renal damage.