May 1, 1992Hypertension
Renal injury from angiotensin II-mediated hypertension.
Key result
Angiotensin II infusion in rats induced marked vascular, glomerular, and tubulointerstitial injury with cell proliferation, leukocyte recruitment, and interstitial fibrosis.
Authors
Discussion
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Implication
Renal arteriolar injury from Ang II in rats is hypothesis-generating; leaves open relevance to human hypertensive kidney disease.
Key Points
- This research investigates the effects of angiotensin II on kidney cells and tissues, focusing on injury mechanisms.
- Infused angiotensin II into rats for 14 days via minipump at 200 ng/min to induce moderate hypertension.
- Analyzed renal tissue for signs of injury, cell proliferation, and phenotypic changes.
- Compared Ang II-infused rats to vehicle-infused control rats for effects on renal function.
- Observed fourfold to 20-fold increase in smooth muscle cell proliferation in renal arterial vessels (p<0.01).
- Identified focal tubulointerstitial injury characterized by tubular atrophy, interstitial fibrosis, and cell proliferation.
- Noted significant upregulation of alpha-smooth muscle actin in renal interstitial cells post Ang II infusion.
PICO
P
Population
Rats infused with Angiotensin II for 14 days to evaluate renal injury.
I
Intervention / Comparator
Angiotensin II vs Vehicle-infused control rats (200 ng/min)
O
Primary Outcome
Renal injury (vascular, glomerular, and tubulointerstitial)
Cite This Study
Johnson et al. (1992) studied Angiotensin II-mediated hypertension. Angiotensin II vs. Vehicle-infused control rats was evaluated on Renal injury (vascular, glomerular, and tubulointerstitial). Angiotensin II infusion in rats induced marked vascular, glomerular, and tubulointerstitial injury with cell proliferation, leukocyte recruitment, and interstitial fibrosis.