Key Points
- To determine the molecular mechanisms regulating intrarenal angiotensin II generation by analyzing renin, angiotensinogen, and kallikrein gene expression in experimental models of hypertension.
- Evaluated two-kidney, one clip (2K1C) Goldblatt hypertensive rats and uninephrectomized rats infused with angiotensin II (40 ng/min via osmotic minipump) after 14 days.
- Measured intrarenal renin mRNA levels, renal and hepatic angiotensinogen mRNA levels, and renal kallikrein gene expression.
- Intrarenal renin mRNA levels increased threefold in clipped kidneys of Goldblatt rats but decreased to 28% of control in nonclipped kidneys and 7% of control in angiotensin II-infused kidneys.
- Angiotensinogen mRNA expression remained sustained at normal levels in both the kidneys and livers of Goldblatt and angiotensin II-infused rats.
- Renal kallikrein gene expression showed no alterations in either hypertensive model 14 days following induction.
Structured PICO
PPopulationUninephrectomized rats and two-kidney, one clip Goldblatt rats
IInterventionChronic low-dose administration of 40 ng/min angiotensin II by osmotic minipump or two-kidney one clip Goldblatt hypertension induction
OOutcomeIntrarenal renin mRNA levels, angiotensinogen mRNA levels, and renal kallikrein gene expressionsurrogate
The study demonstrates differential regulation of renin-angiotensin system genes in experimental hypertension models, with renin mRNA being suppressed by circulating angiotensin II while angiotensinogen mRNA levels are sustained.