|
|
||||||||
NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION
1Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez Mexico City, Mexico; 2Department of Pharmacology, Universidad Antonoma San Luis Potosí, Mexico; 3Hospital Universitario Universidad del Zulia and Centro de Investigaciones Biomédicas, Instituto Venezolano de Investigaciones Cientifica Zulia, Maracaibo, Venezuela; and 4Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida
Submitted 13 September 2006 ; accepted in final form 26 April 2007
Renal immune cell infiltration and cells expressing angiotensin II (AII) in tubulointerstitial areas of the kidney are features of experimental models of salt-sensitive hypertension (SSHTN). A high-salt intake tends to suppress circulating AII levels, but intrarenal concentrations of AII have not been investigated in SSHTN. This study explored the relationship between these features to gain insight into the pathophysiology of SSHTN. Plasma angiotensin II (AII) and renal interstitial AII (microdialysis technique) and the infiltration of macrophages, lymphocytes, and AII-positive cells were determined in SSHTN induced by 5 wk of a high-salt diet (HSD) after short-term infusion of AII in rats with (n = 10) and without (n = 11) treatment with mycophenolate mofetil (MMF) and in control rats fed a high- (n = 7) and normal (n = 11) salt diet. As in previous studies, MMF did not affect AII-associated hypertension but reduced the interstitial inflammation and the SSHTN in the post-AII-period. During the HSD period, the AII group untreated with MMF had mean ± SD) low plasma (2.4 ± 1.4 pg/ml) and high interstitial AII concentration (1,310 ± 208 pg/ml); MMF treatment resulted in a significantly lower interstitial AII (454 ± 128 pg/ml). Renal AII concentration and the number of tubulointerstitial AII-positive cells were correlated. Blood pressure correlated positively with interstitial AII and negatively with plasma AII, thus giving compelling evidence of the paramount role of the AII within the kidney in the AII-induced model of salt-driven hypertension.
lymphocytes; macrophages; renal hypertension
This article has been cited by other articles:
![]() |
B. Ponnuchamy and R. A. Khalil Cellular mediators of renal vascular dysfunction in hypertension Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R1001 - R1018. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Rodriguez-Iturbe, N. D. Vaziri, and R. J. Johnson Inflammation, Angiotensin II, and Hypertension Hypertension, November 1, 2008; 52(5): e135 - e135. [Full Text] [PDF] |
||||
![]() |
L. G. Sanchez-Lozada, V. Soto, E. Tapia, C. Avila-Casado, Y. Y. Sautin, T. Nakagawa, M. Franco, B. Rodriguez-Iturbe, and R. J. Johnson Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia Am J Physiol Renal Physiol, October 1, 2008; 295(4): F1134 - F1141. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Stewart, I. Taneja, N. Raghunath, D. Clarke, and M. S. Medow Intradermal angiotensin II administration attenuates the local cutaneous vasodilator heating response Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H327 - H334. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |