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1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana, United States
2 Department of Physiology, SL39, Tulane University School of Medicine, New Orleans,, Louisiana, United States
* To whom correspondence should be addressed. E-mail: hkobori{at}tulane.edu.
Chronic angiotensin (Ang) II infusions into rats lead to augmented intrarenal levels of AngII and inflammatory factors, impaired renal function, and progressive hypertension. Residual effects persist after cessation of AngII infusions as manifested by a hypertensive response to high salt intake. This study was performed to determine the residual cytokines and chemokines following the cessation of AngII infusion. Male Sprague-Dawley rats, maintained on a normal diet, received either a sham operation or continuous AngII infusion (120 ng/min) subcutaneously via minipumps. The AngII-infused rats were further subdivided into 3 subgroups. Minipumps were removed on day 12 with subsequent harvesting of kidneys at 0, 3 and 6 days after cessation of AngII infusion. After 12 days of AngII infusion, systolic blood pressure (BP), interstitial fibrosis, preglomerular hypertrophy, and interstitial macrophage infiltration were significantly enhanced compared to the shams. By 3 days following the cessation of AngII infusion, systolic BP was normalized; however, interstitial fibrosis and preglomerular hypertrophy were still present. Furthermore, increased interstitial macrophage infiltration was still present 6 days after cessation of AngII infusion. Importantly, augmented mRNA levels of monocyte chemotactic protein (MCP)-1 (1.55±0.15 vs 1.00±0.13, relative ratio) and transforming growth factor-beta (TGF-b) 1 (1.52±0.16 vs 1.00±0.08) persisted 6 days after the withdrawal of AngII infusion (1.60±0.20 for MCP-1 and 1.43±0.17 for TGF-b1). Thus, the AngII-induced activation of MCP-1 and TGF-b1 is sustained and may account for the persistent effect of chronic AngII infusions on interstitial macrophage infiltration, suggesting a possible mechanism for the development of salt sensitivity in AngII-dependent hypertension.
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