Abstract
Estrogen has been implicated in renal protection afforded females with hypertension. Nitric oxide (NO) is an important regulator of kidney function, and NO levels have are reported to be higher in females. The hypothesis of this study was that estrogen enhances the NO system in the renal cortex of SHR. 14-week old female SHR were studied (n=3–8): gonad-intact, ovariectomized (OVX), and OVX with estrogen replacement (OVXE, 1.7 mg/pellet). Microalbumin (ualb) excretion was used to assess renal injury. OVXE had greater ualb excretion (1.8±0.2 ug/day/gram) compared to intact and OVX (0.8±0.1, 0.6±0.1 ug/day/gram respectively, p=0.003). Nitrite/nitrate (NOx) excretion and NOS protein expression and activity were examined in the renal cortex. NOx excretion was comparable between groups (pmol/day: intact 6.5±0.7, OVX 7.3±0.8, OVXE 6.2±0.7). NOS3 protein expression and phosphorylation of NOS3 on serine residues 1177 and 633 were comparable in all groups. However, NOS1 expression was greater in the cortex from intact females (2.38±.18 RDU) compared to OVX and OVXE (RDU: OVX 1.19±0.24, OVXE 0.67±0.02; p=0.04 vs intact, OVX vs OVXE p=0.09). There was no difference in total NOS activity between groups (pmol/mg: intact 21.1±4.4, OVX 18.9±1.9, OVXE 25.4±7.4). These data suggest that unopposed estrogen does not protect against renal injury. Furthermore, renal cortical NOS1 is sensitive to a non-estrogen ovarian hormone.
Published Version
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