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.
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.
Several experimental procedures produce dramatic alterations in kidney renin production, leading to increased plasma renin levels with attendant hypertension in animal model systems. The pattern of changes for kidney renin messenger RNA (mRNA) levels relative to changes for tissue and plasma renin activity was studied in Sprague-Dawley rats made hypertensive by either coarctation of the aorta between the two renal arteries or clipping of the left renal artery. In both models, the renin mRNA content of the contralateral hypertrophied kidney transiently decreased to undetectable levels while the ischemic kidney exhibited transient increases in renin mRNA. In aorta-coarctated rats ischemic kidney renin mRNA increased 10-fold to 16-fold during the first 3 days after coarctation but returned to the level observed in sham-operated rats 14 days after operation. However, differences between the time course and magnitude of changes in renin mRNA levels and the pattern of alteration in tissue and plasma renin activities were observed. Thus, although the kidney renin mRNA transiently increased in hypertensive animals, the extent of this increase was insufficient to account for the 30-fold to 50-fold increases in plasma renin activity. Similarly, the transient increase in kidney renin mRNA was inconsistent with only a twofold increase in tissue renin enzyme activity of the ischemic kidney. These data indicate that in addition to alterations in the kidney renin mRNA pool, posttranslational processing and/or release of renin from the kidney are cocontributors in regulating the plasma renin levels in these experimental models.
Moffett et al. (Wed,) conducted a other in 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.