scholarly journals Altered Expression and Function of Hepatic Transporters in a Rodent Model of Polycystic Kidney Disease

2019 ◽  
Vol 47 (8) ◽  
pp. 899-906 ◽  
Author(s):  
Jacqueline Bezençon ◽  
James J. Beaudoin ◽  
Katsuaki Ito ◽  
Dong Fu ◽  
Sharin E. Roth ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Rodent Model ◽  
Polycystic Kidney ◽  
Altered Expression ◽  
Hepatic Transporters ◽  
And Function

scholarly journals SAT-331 RENAL DENERVATION DOES NOT REDUCE BLOOD PRESSURE IN A RODENT MODEL OF POLYCYSTIC KIDNEY DISEASE

2019 ◽  
Vol 4 (7) ◽  
pp. S146
Author(s):  
S. Li ◽  
C.M. Hildreth ◽  
A.A. Rahman ◽  
V.J. Tallapragada ◽  
P.M. Pilowsky ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Renal Denervation ◽  
Reduce Blood Pressure ◽  
Rodent Model ◽  
Polycystic Kidney

751 TREATMENT WITH THE ANTIOXIDANT TEMPOL DOES NOT SIGNIFICANTLY AMELIORATE HYPERTENSION OR PROGRESSION OF RENAL DISEASE IN A RODENT MODEL OF POLYCYSTIC KIDNEY DISEASE

2012 ◽  
Vol 30 ◽  
pp. e217
Author(s):  
Jacqueline K. Phillips ◽  
Alice Ding ◽  
Priyadharshani Kalaignanasundaram ◽  
Sharon D. Ricardo ◽  
Amany Abdelkader ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Polycystic Kidney Disease ◽  
Rodent Model ◽  
Polycystic Kidney ◽  
Progression Of Renal Disease

Heightened epithelial Na+ channel-mediated Na+ absorption in a murine polycystic kidney disease model epithelium lacking apical monocilia

2006 ◽  
Vol 290 (4) ◽  
pp. C952-C963 ◽  
Author(s):  
Dragos Olteanu ◽  
Bradley K. Yoder ◽  
Wen Liu ◽  
Mandy J. Croyle ◽  
Elisabeth A. Welty ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Collecting Duct ◽  
Short Circuit ◽  
Na Channel ◽  
Cortical Collecting Duct ◽  
Polycystic Kidney ◽  
Luminal Membrane ◽  
And Function ◽  
Amiloride Analogs

The Tg737° rpk autosomal recessive polycystic kidney disease (ARPKD) mouse carries a hypomorphic mutation in the Tg737 gene. Because of the absence of its protein product Polaris, the nonmotile primary monocilium central to the luminal membrane of ductal epithelia, such as the cortical collecting duct (CCD) principal cell (PC), is malformed. Although the functions of the renal monocilium remain elusive, primary monocilia or flagella on neurons act as sensory organelles. Thus we hypothesized that the PC monocilium functions as a cellular sensor. To test this hypothesis, we assessed the contribution of Polaris and cilium structure and function to renal epithelial ion transport electrophysiology. Properties of Tg737° rpk mutant CCD PC clones were compared with clones genetically rescued with wild-type Tg737 cDNA. All cells were grown as polarized cell monolayers with similarly high transepithelial resistance on permeable filter supports. Three- to fourfold elevated transepithelial voltage ( Vte) and short-circuit current ( Isc) were measured in mutant orpk monolayers vs. rescued controls. Pharmacological and cell biological examination of this enhanced electrical end point in mutant monolayers revealed that epithelial Na+ channels (ENaCs) were upregulated. Amiloride, ENaC-selective amiloride analogs (benzamil and phenamil), and protease inhibitors (aprotinin and leupeptin) attenuated heightened Vte and Isc. Higher concentrations of additional amiloride analogs (ethylisopropylamiloride and dimethylamiloride) also revealed inhibition of Vte. Cell culture requirements and manipulations were also consistent with heightened ENaC expression and function. Together, these data suggest that ENaC expression and/or function are upregulated in the luminal membrane of mutant, cilium-deficient orpk CCD PC monolayers vs. cilium-competent controls. When the genetic lesion causes loss or malformation of the monocilium, ENaC-driven Na+ hyperabsorption may explain the rapid emergence of severe hypertension in a majority of patients with ARPKD.

scholarly journals Renal denervation does not affect hypertension or the renin-angiotensin system in a rodent model of juvenile-onset polycystic kidney disease: clinical implications

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sheran Li ◽  
Cara M. Hildreth ◽  
Ahmed A. Rahman ◽  
Sean A. Barton ◽  
Benjamin F. Wyse ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Renal Denervation ◽  
Renin Angiotensin System ◽  
Rodent Model ◽  
Angiotensin Ii Receptor ◽  
Polycystic Kidney ◽  
Juvenile Onset ◽  
Angiotensin System ◽  
Renin Angiotensin

AbstractWe examined the effect of total and afferent renal denervation (RDN) on hypertension and the renin-angiotensin system (RAS) in a rodent model of juvenile-onset polycystic kidney disease (PKD). Lewis Polycystic Kidney (LPK) and control rats received total, afferent or sham RDN by periaxonal application of phenol, capsaicin or normal saline, respectively, and were monitored for 4-weeks. Afferent RDN did not affect systolic blood pressure (SBP) determined by radiotelemetry in either strain (n = 19) while total RDN significantly reduced SBP in Lewis rats 4-weeks post-denervation (total vs. sham, 122 ± 1 vs. 130 ± 2 mmHg, P = 0.002, n = 25). Plasma and kidney renin content determined by radioimmunoassay were significantly lower in LPK vs. Lewis (plasma: 278.2 ± 6.7 vs. 376.5 ± 11.9 ng Ang I/ml/h; kidney: 260.1 ± 6.3 vs. 753.2 ± 37.9 ng Ang I/mg/h, P < 0.001, n = 26). These parameters were not affected by RDN. Intrarenal mRNA expression levels of renin, angiotensinogen, angiotensin-converting enzyme (ACE)2, and angiotensin II receptor type 1a were significantly lower, whereas ACE1 expression was significantly higher in the LPK vs. Lewis (all P < 0.05, n = 26). This pattern of intrarenal RAS expression was not changed by RDN. In conclusion, RDN does not affect hypertension or the RAS in the LPK model and indicates RDN might not be a suitable antihypertensive strategy for individuals with juvenile-onset PKD.

scholarly journals Altered Hepatobiliary Disposition of Tolvaptan and Selected Tolvaptan Metabolites in a Rodent Model of Polycystic Kidney Disease

2018 ◽  
Vol 47 (2) ◽  
pp. 155-163 ◽  
Author(s):  
James J. Beaudoin ◽  
Jacqueline Bezençon ◽  
Yanguang Cao ◽  
Katsuhiko Mizuno ◽  
Sharin E. Roth ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Rodent Model ◽  
Polycystic Kidney ◽  
Hepatobiliary Disposition

scholarly journals Kidney volume and function in autosomal dominant polycystic kidney disease

2013 ◽  
Vol 18 (1) ◽  
pp. 157-165 ◽  
Author(s):  
Eiji Higashihara ◽  
Kikuo Nutahara ◽  
Takatsugu Okegawa ◽  
Toshihide Shishido ◽  
Mitsuhiro Tanbo ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
And Function
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