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1 Hypertension Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
2 Hypertension Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
* To whom correspondence should be addressed. E-mail: mchappel{at}wfubmc.edu.
Estrogen depletion markedly exacerbates hypertension in female congenic mRen2.Lewis rats, a model of tissue renin overexpression. Since estrogen influences nitric oxide synthase (NOS) and NO may exert differential effects on blood pressure, the present study investigated the functional expression of NOS isoforms in the kidney of ovariectomized (OVX) mRen2.Lewis rats. OVX- mRen2.Lewis exhibited an increase in systolic blood pressure (SBP) of 171 ±5 vs. 141 ± 7 mmHg (p<0.01) for intact littermates. Renal cortical mRNA and protein levels for endothelial NOS (eNOS) were reduced 50-60% (p<0.05) and negatively correlated with blood pressure. In contrast, cortical neuronal NOS (nNOS) mRNA and protein levels increased 100 to 300% (p<0.05). In the OVX kidney, nNOS immunostaining was more evident in the macula densa, cortical tubules and the medullary collecting ducts as compared to the intact group. To determine whether the increase in renal nNOS expression constitutes a compensatory response to the reduction in renal eNOS, we treated both intact and OVX mRen2.Lewis with the selective nNOS inhibitor L-VNIO from 11 to 15 weeks of age. The nNOS inhibitor reduced blood pressure in the OVX group (185 ±3 vs. 151 ± 8 mmHg, p<0.05), but pressure was not altered in the intact group (146 ± 4 vs. 151 ± 4 mmHg). In summary, exacerbation of blood pressure in the OVX mRen2.Lewis rats was associated with the discoordinate regulation of renal NOS isoforms. Estrogen sensitivity in this congenic strain may involve the influence of NO through the regulation of both eNOS and nNOS.
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