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May 1, 2000HypertensionOpen Access

Local Angiotensin II and Transforming Growth Factor-β1 in Renal Fibrosis of Rats

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Why the study?

Does aldosterone-induced renal injury increase local ACE, Ang II receptors, and TGF-beta1 expression in rats?

Population

Rat model of renal injury with subsequent fibrosis created with chronic elevations in circulating…

Comparison

Uninephrectomy followed by aldosterone and 1%… vs Normal rats serving as controls

Design

Preclinical

Follow-up

6 weeks

Authors

YSYao SunTianjin Medical University Cancer Institute and HospitalJZJiakun ZhangTongji HospitalJZJohn Q. ZhangThe University of Texas at San Antonio

Discussion

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Implication

May implicate local renin-angiotensin-TGF-beta1 axis in aldosterone-driven renal fibrosis; leaves open translation to human disease.

Key Points

  • To determine the spatial localization and receptor binding density of ACE and angiotensin II relative to TGF-β1 mRNA, type I collagen mRNA, and myofibroblasts during renal fibrosis.
  • Evaluated uninephrectomized rats receiving aldosterone infusion (0.75 µg/h subcutaneously) and 1% NaCl drinking water for 6 weeks alongside intact control rats (n=7 per group).
  • Measured blood pressure, plasma renin activity, and plasma creatinine levels.
  • Quantified the tissue distribution and binding density of ACE, AT1 and AT2 receptors, TGF-β1 mRNA, type I collagen mRNA, and myofibroblasts at sites of renal injury.
  • Aldosterone-treated rats developed significant hypertension, suppressed plasma renin activity, elevated plasma creatinine, and diffuse cortical and medullary fibrosis with abundant myofibroblasts (P<0.01 vs controls).
  • Binding density of ACE and Ang II receptors (60% AT1, 40% AT2) increased significantly at sites of renal fibrosis compared to controls (P<0.01).
  • Expression of TGF-β1 mRNA and type I collagen mRNA increased markedly and co-localized at identical sites of fibrous tissue formation (P<0.01).

Structured PICO

Does aldosterone-induced renal injury increase local ACE, Ang II receptors, and TGF-beta1 expression in rats?

P
Population
Rat model of renal injury with subsequent fibrosis created with chronic elevations in circulating aldosterone (ALDO). Two groups (n=7 each): normal rats and uninephrectomized rats.
I
Intervention
Uninephrectomy followed by aldosterone (0.75 microg/h SC) and 1% NaCl in drinking water for 6 weeks
C
Comparator
Normal rats serving as controls
O
Outcome
Distribution and binding density of ACE and Ang II receptors in repairing kidneys, and their anatomic relationship to TGF-beta1 mRNA, type I collagen mRNA, collagen accumulation, and myofibroblastssurrogate

In a rat model of renal repair, enhanced expression of ACE, Ang II receptors, and TGF-beta1 is associated with renal fibrosis, suggesting autocrine/paracrine functions of local Ang II.

Cite This Study

Sun et al. (2000) studied this question.

synapsesocial.com/papers/6a770d05d2fa2470761e9b86https://doi.org/10.1161/01.hyp.35.5.1078
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Role of angiotensin II in renal injury of deoxycorticosterone acetate-salt hypertensive rats.1994 · 117 citations
  2. 2Renal renin-angiotensin system in diabetes: functional, immunohistochemical, and molecular biological correlations1993 · 310 citations
  3. 3LOCALIZATION OF ANGIOTENSIN CONVERTING ENZYME IN RAT FOREBRAIN AND OTHER TISSUES BY IN VITRO AUTORADIOGRAPHY USING 125‐I‐LABELLED MK351A1984 · 51 citations
  4. 4Characterization of cardiac angiotensin converting enzyme (ACE) andin vivoinhibition following oral quinapril to rats1990 · 39 citations
  5. 5Prevention of experimental cyclosporin-induced interstitial fibrosis by losartan and enalapril1995 · 143 citations