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J Am Soc Nephrol 12:2263-2271, 2001
© 2001 American Society of Nephrology

Renal Cortical Vasoconstriction Contributes to Development of Salt-Sensitive Hypertension after Angiotensin II Exposure

MARTHA FRANCO*, EDILIA TAPIA*, JOSÉ SANTAMARÍA*, IGNACIO ZAFRA*, ROMEO GARCÍA-TORRES*, KATHERINE L. GORDON{dagger}, HÉCTOR PONS{dagger}, BERNARDO RODRÍGUEZ-ITURBE{ddagger}, RICHARD J. JOHNSON{dagger} and JAIME HERRERA-ACOSTA*

* Department of Nephrology, Instituto Nacional de Cardiología, Mexico City, Mexico
{dagger} Division of Nephrology, University of Washington Medical Center, Seattle, Washington
{ddagger} Instituto de Investigaciones Biomédicas, Maracaibo, Venezuela.

Address correspondence to Dr. Martha Franco, Nephrology Department, Instituto Nacional de Cardiología, Juan Badiano No. 1, Mexico City, Tlalpan 14080, Mexico. Phone: 525-573-6902; Fax: 525-573-7716; E-mail: marthafranco{at}eudoramail.com

Abstract. Rats that are administered angiotensin II (AngII) for 2 wk develop persistent salt-sensitive hypertension, which can be prevented by the immunosuppressor mycophenolate mofetil (MMF) given during the AngII infusion. This study examined the contribution of glomerular hemodynamics (GFR dynamics) in the post-AngII hypertensive response to a high-salt diet (HSD) and the effect of MMF treatment. During AngII administration, rats developed severe hypertension (systolic BP [SBP], 185 ± 3.9 mmHg), proteinuria, afferent and efferent vasoconstriction, and glomerular hypertension. Rats that received AngII+MMF showed similar responses to AngII; however, they developed lower proteinuria (P < 0.05). At 2 wk, AngII was withdrawn and SBP returned toward normal. Rats were then placed on an HSD (4% NaCl), resulting in a progressive increase in SBP (155 ± 8.2 mmHg at week 1 and 163 ± 4.5 mmHg at week 5). GFR dynamic alterations persisted after AngII was stopped, i.e., afferent and efferent vasoconstriction, decreased glomerular plasma flow and single-nephron GFR, and lower ultrafiltration coefficient. These changes correlated with the thickening of the afferent arteriole and with focal tubulointerstitial injury. In the AngII+MMF group, SBP remained unchanged throughout the HSD period (146 ± 2.3 mmHg at week 1 and 148 ± 4.4 mmHg at week 5) in association with less afferent arteriolar thickening and tubulointerstitial injury. Single-nephron GFR, glomerular plasma flow, efferent resistance, and ultrafiltration coefficient returned to normal with a significant reduction in afferent resistance. These results suggest a critical role of cortical vasoconstriction in salt-sensitive hypertension. The MMF-induced prevention of these changes suggests that immune mechanisms are involved in the vasoconstrictive response.




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