The role of angiotensin converting enzyme 2 in the generation of angiotensin 1–7 by rat proximal tubules

Li, Ningjun; Zimpelmann, Joseph; Cheng, Keding; Wilkins, John A.; Burns, Kevin D.

doi:10.1152/ajprenal.00144.2004

Cited by 133 publications

(158 citation statements)

References 32 publications

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“…On the other hand, with the above mentioned commercially available goat polyclonal anti-ACE2 antibody, ACE2-positive staining was subsequently reported to be present not only in tubular segments, but also in glomeruli and endothelial cells of male adult SD rats. 25 Similarly, in adult SHR and WKY rats, ACE2 mRNA and protein was present in proximal tubuli and large vessels with weak distal tubular and glomerular presence using the initial rabbit polyclonal anti-ACE2. 26 Considering these between-laboratory discrepancies, in the current study we took great care to rigorously test validity and reproducibility of our immunohistochemistry data.…”

Section: Controlsmentioning

confidence: 91%

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Renal ACE2 expression and activity is unaltered during established hypertension in adult SHRSP and TGR(mREN2)27

et al. 2009

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Differential renal expression of a homolog of the angiotensin-converting enzyme (ACE), that is, ACE2, has been implicated as a genetic basis of polygenetic hypertension in the stroke-prone spontaneously hypertensive rat model. However, data on the role of ACE2 in hypertension are still inconclusive. Therefore, we analyzed kidney ACE2 mRNA, ACE2 protein and ACE2 enzyme activities in the adult polygenetic stroke-prone spontaneously hypertensive rat (SHRSP) and the monogenetic TGR(mREN2)27 rat models, in comparison with their normotensive reference strains, Wistar-Kyoto (WKY) and Spraque-Dawley (SD) rats, respectively. Kidney ACE2 mRNA was studied using quantitative real-time reverse transcriptase-PCR (RT-PCR) in cortex and medulla, whereas protein expression was scored semiquantitatively in detail in different renal structures using immunohistochemistry. Furthermore, total renal tissue ACE2 activity was measured using a fluorimetric assay that was specified by the ACE2 inhibitor DX600. In SHRSP and homozygous TGR(mREN2)27 rats with established hypertension, kidney ACE2 mRNA, protein and tissue ACE2 activities were not different from their respective WKY and SD reference strain, respectively. In addition, when we looked at renal localization, we found ACE2 protein to be predominantly present in glomeruli and endothelium with weak staining in distal and negative staining in proximal tubuli. Thus, our data challenge previous work that implicates ACE2 as a candidate gene for hypertension in SHRSP by reporting a significant reduction of ACE2 in the kidneys of SHRSP. Taken together, renal ACE2 is not altered in the SHRSP and TGR(mREN2)27 genetic rat models with established hypertension.

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Section: Controlsmentioning

confidence: 91%

“…28,29 Besides, kinetic differences in AngI and AngII metabolism are shown to be exist between rat, human and sheep kidneys. 25,30,31 There are some limitations to our study. First, our data were obtained in adult animals with established hypertension and hence do not rule out a role for renal ACE2 in the early onset of hypertension.…”

Section: Controlsmentioning

confidence: 97%

Renal ACE2 expression and activity is unaltered during established hypertension in adult SHRSP and TGR(mREN2)27

et al. 2009

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“…Activation of Mas, the G-protein-coupled Ang (1-7) receptor, triggers vasodilation and antifibrotic signaling mechanisms in cardiac myocytes [15] . In this alternative pathway, ACE2 converts Ang II to Ang (1-7) and Ang I to Ang (1-9) [16] .…”

Section: Introductionmentioning

confidence: 99%

Telmisartan attenuates hepatic fibrosis in bile duct-ligated rats

Liu

Wen

et al. 2012

Acta Pharmacol Sin

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Aim: To evaluate the antifibrotic effect of telmisartan, an angiotensin II receptor blocker, in bile duct-ligated rats. Methods: Adult Sprague-Dawley rats were allocated to 3 groups: sham-operated rats, model rats underwent common bile duct ligation (BDL), and BDL rats treated with telmisartan (8 mg/kg, po, for 4 weeks). The animals were sacrificed on d 29, and liver histology was examined, the Knodell and Ishak scores were assigned, and the expression of angiotensin-converting enzyme (ACE) and ACE2 was evaluated with immunohistochemical staining. The mRNAs and proteins associated with liver fibrosis were evaluated using RTQ-PCR and Western blot, respectively. Results: The mean fibrosis score of BDL rats treated with telmisartan was significantly lower than that of the model rats (1.66±0.87 vs 2.13±0.35, P=0.015). However, there was no significant difference in inflammation between the two groups, both of which showed moderate inflammation. Histologically, treatment with telmisartan significantly ameliorated BDL-caused the hepatic fibrosis. Treatment with telmisartan significantly upregulated the mRNA levels of ACE2 and MAS, and decreased the mRNA levels of ACE, angiotensin II type 1 receptor (AT1-R), collagen type III, and transforming growth factor β1 (TGF-β1). Moreover, treatment with telmisartan significantly increased the expression levels of ACE2 and MAS proteins, and inhibited the expression levels of ACE and AT1-R protein. Conclusion:Telmisartan attenuates liver fibrosis in bile duct-ligated rats via increasing ACE2 expression level.

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“…In the kidney, ACE2 gene expression has been observed in glomeruli, the vasa recta and all nephron segments except for the thick ascending limb [171]. Additionally, relatively high amounts of ACE2 were detected in the apical brush-border membrane of proximal tubule epithelia, where it colocalized with ACE [171].…”

Section: Synthesis Of Ang-(1-7)mentioning

confidence: 99%

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Mello-Aires¹,

Dellova²,

Castelo‐Branco³

et al. 2017

Nephrol Renal Dis

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This article reviews the main body of knowledge regarding NHE1 and NHE3 exchangers and their interaction with Angiotensin II, Angiotensin-(1-7), Aldosterone and Arginine Vasopressin, particularly their renal actions. This work addresses the biphasic effects of different hormonal doses on NHE1 or NHE3 in proximal tubule in Wistar, SHR (hypertensives) and their control WKY (normotensives) rats or MDCK cells (which share similarities with the collecting duct). The hormones were applied alone, with their inhibitors or plus agents that change the [Ca 2+ ]i. The data are compatible with hormonal stimulation of these exchangers by increases of [Ca 2+ ]i in lower range, and inhibition at high [Ca 2+ ]i. In MDCK cells and Wistar rats, low doses of ANG II, ALDO or AVP stimulated the exchangers, while high doses inhibited them. ANG-(1-7), in Wistar or WKY rats has inverse, dose-dependent effects. In SHR rats, the biphasic effects of ANG-(1-7) were similar to the effects of ANG II, ALDO or AVP in Wistar rats. The interactions between these effects may represent a mechanism that regulates extracellular volume. In hypertensives animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated hypertension. Figure 6 shows a schematic model to describe these biphasic hormonal effects.

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The role of angiotensin converting enzyme 2 in the generation of angiotensin 1–7 by rat proximal tubules

Cited by 133 publications

References 32 publications

Renal ACE2 expression and activity is unaltered during established hypertension in adult SHRSP and TGR(mREN2)27

Renal ACE2 expression and activity is unaltered during established hypertension in adult SHRSP and TGR(mREN2)27

Telmisartan attenuates hepatic fibrosis in bile duct-ligated rats

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

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