The hypertensive mRen2.Lewis rats exhibited higher ANG II in kidney cortical and medullary regions, with lower cortical nuclear and medullary plasma membrane AT1 sites compared to Lewis controls.
The hypertensive mRen2.Lewis rat model demonstrates elevated intrarenal ANG II levels and a compensatory downregulation of AT1 receptors in the kidney.
We established a new congenic model of hypertension, the mRen(2). Lewis rat and assessed the intracellular expression of angiotensin peptides and receptors in the kidney. The congenic strain was established from the backcross of the (mRen2)27 transgenic rat that expresses the mouse renin 2 gene onto the Lewis strain. The 20-wk-old male congenic rats were markedly hypertensive compared with the Lewis controls (systolic blood pressure: 195 +/- 2 vs. 107 +/- 2 mmHg, P 200 fmol/mg protein) and affinity for the sarthran ligand (KD95%) were the AT1 receptor subtype. CORT ANG II receptor Bmax and KD values in nuclei were 75 and 50% lower, respectively, for the mRen2. Lewis vs. the Lewis rats. In the MED, the PM receptor density (Lewis: 50 +/- 4 vs. mRen2. Lewis: 21 +/- 5 fmol/mg protein) and affinity (Lewis: 0.31 +/- 0.1 vs. 0.69 +/- 0.1 nM) were lower in the mRen2. Lewis rats. In summary, the hypertensive mRen2. Lewis rats exhibit higher ANG II in both CORT and MED regions of the kidney. Evaluation of intracellular ANG II receptors revealed lower CORT NUC and MED PM AT1 sites in the mRen2. Lewis. The downregulation of AT1 sites in the mRen2. Lewis rats may reflect a compensatory response to dampen the elevated levels of intrarenal ANG II.
Pendergrass et al. (Wed,) conducted a other in Hypertension. mRen2.Lewis rat model vs. Lewis controls was evaluated on Intracellular expression of angiotensin peptides and receptors in the kidney. The hypertensive mRen2.Lewis rats exhibited higher ANG II in kidney cortical and medullary regions, with lower cortical nuclear and medullary plasma membrane AT1 sites compared to Lewis controls.