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Articles in PresS, published online ahead of print July 24, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00199.2002
Submitted on May 22, 2002
Accepted on July 17, 2002
1 Renal Service and Laboratory, Instituto de Investigaciones Biomedicas (INBIOMED), Hospital Universitario, Universidad del Zulia, Maracaibo, Zulia, Venezuela
* To whom correspondence should be addressed. E-mail: bri{at}iamnet.com.
Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated if proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2g of bovine serum albumin intraperitoneally daily for 2 weeks. Following protein overload (PO), six weeks of a high salt diet induced hypertension (systolic blood pressure, SBP= 156 ± 11.8 mmHg) while rats that remained on a normal salt diet and control rats (without PO) on a high salt diet were normotensive. Administration of mycophenolate mofetil (20mg/kg/day) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II positive cells and oxidative stress (superoxide positive cells and renal malondialdehyde content) and in resistance to the hypertensive effect of the high salt diet (SBP= 129 ± 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.
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