Key result
Aorta coarctation or renal artery clipping transiently increased ischemic kidney renin mRNA 10- to 16-fold, which was insufficient to account for the 30- to 50-fold increase in plasma renin activity.
Population
Sprague-Dawley rats made hypertensive by either coarctation of the aorta between the two renal arteries or…
Comparison
Experimentally induced hypertension via… vs Sham-operated rats
Design
Preclinical
Follow-up
14 days
Authors
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Posttranslational renin mechanisms may predominate in experimental hypertension; leaves open dominant pathways and human relevance.
In experimental hypertension models, transient increases in kidney renin mRNA are insufficient to explain the massive increases in plasma renin activity, suggesting posttranslational processing or release mechanisms are key contributors.
Moffett et al. (1986) studied Experimentally induced hypertension. Coarctation of the aorta or clipping of the left renal artery vs. Sham-operated rats was evaluated on Kidney renin messenger RNA (mRNA) levels, tissue and plasma renin activity. Aorta coarctation or renal artery clipping transiently increased ischemic kidney renin mRNA 10- to 16-fold, which was insufficient to account for the 30- to 50-fold increase in plasma renin activity.
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