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1 Nephrology, Instituto Nacional de Cardiologia I.Ch., Mexico City, DF, Mexico
2 Pharmacology, UASLP, San Luis Potosi, SLP., Mexico
3 Nephrology, Hospital Universitario de Maracaibo, Maracaibo, ZULIA, Venezuela
4 Division of nephrology, Hypertension and transplantation, University of Florida, Gainesville, Florida, United States; University of Florida, 1600 S.W. Archer Rd., Gainesville, Florida, 32610, United States
5 Nephrology, Instituto Nacional de Cardiologia I. Ch., Mexico City, DF, Mexico
6 Pharmacology, UASLP, San Luis Potosi, SLP, Mexico
7 Nephrology, Instituto Nacional de cardiologia I.Ch., Mexico City, DF, Mexico
* To whom correspondence should be addressed. E-mail: marthafranco{at}lycos.com.
Transient administration of angiotensin II (AngII) causes persistent salt-sensitive hypertension associated with arteriolopathy, interstitial inflammation, and cortical vasoconstriction; blocking the vascular and inflammatory changes with mycophenolate mofetil (MMF) prevents vasoconstriction. While infiltrating leukocytes during the salt-sensitive hypertension phase express angiotensin II, the functional role of angiotensin II during this phase is not known. We examined the acute effect of candesartan on renal hemodynamics during the established salt-sensitive hypertensive phase and related these findings to direct measurement of intrarenal angiotensin II and inflammatory cells in rats previously exposed to angiotensin II with or without MMF treatment. Sham controls were also examined. The administration of angiotensin II, followed by exposure to high salt diet, resulted in hypertension, cortical vasoconstriction, an increase in interstitial inflammatory cells (44.8±1.3 lymphocytes/mm2, and 30.8±1.2 macrophages/mm2 AngII vs. 19.6±2 lymphocytes/mm2, and 22±0.7 macrophages/mm2 Sham) and increase in renal angiotensin II levels (1358±74.6 pg/ml AngII vs. 194±9.28 pg/ml Sham). Treatment with MMF during the administration of exogenous angiotensin II resulted in reduction in renal interstitial inflammation (19.7±0.9 lymphocytes/mm2 and 15.9±0.8 machophages/mm2), angiotensin II levels, (436.9±52.29 pg/ml), cortical vasoconstriction and stable blood pressure levels during the subsequent challenge with a high salt diet. Acute administration of candesartan similarly reduced renal vasoconstriction and blood pressure. We conclude that the cortical vasoconstriction occurring with salt-sensitive hypertension following exposure to angiotensin II is mediated by intrarenal angiotensin II, related, at least in part, to the interstitial inflammation.
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