Renal Endothelin ET A /ET B Receptor Imbalance Differentiates Salt-Sensitive From Salt-Resistant Spontaneous Hypertension

Publisher Website
Google Scholar
Abstract
It is unclear why a subgroup of patients with essential hypertension develop salt-sensitive hypertension with progression of target organ damage over time. We evaluated the role of the renal endothelin (ET) system in the stroke-prone spontaneously hypertensive rat (SHRSP) model of salt-sensitive spontaneous hypertension (SS-SH) compared with the spontaneously hypertensive rat (SHR) model of salt-resistant spontaneous hypertension (SR-SH). Both strains were studied after either sham-operation on a normal diet (Sham) or after unilateral nephrectomy and high NaCl loading (NX-NaCl) with 4% NaCl in diet for 6 weeks (n=10, respectively). Systolic blood pressure (SBP) increased only in SHRSP-NX-NaCl compared with SHRSP-Sham (250±6 versus 172±5 mm Hg, P P Na + ) was significantly reduced by 38% in SHRSP-NX-NaCl compared with SHR-NX-NaCl ( P A and ET B receptor densities after NX-NaCl (2.2-fold, P A compared with ET B binding (4.7-fold versus 2.4-fold, P A /ET B receptor ratio only in the SHRSP-NX-NaCl ( P A /ET B receptor ratio may contribute to the development and progression of SS-SH.

This publication has 6 references indexed in Scilit: