Abstract
We designed experiments to test the hypothesis that Dahl salt-sensitive (SS) rats are sensitive to high-fat diet (HFD)–induced hypertension and renal injury via an inflammatory mechanism. Twelve-week-old Dahl SS rats were maintained on a normal diet (ND; 14% fat), HFD (59% fat), or HFD supplemented with the lymphocyte immunosuppressive agent, mycophenolate mofetil (HFD + MMF; 30 mg/kg/day orally in diet), for a period of 4 weeks. Mean arterial pressure (MAP), metabolic parameters, T lymphocyte (CD3+) localization, and renal structural damage were assessed during the studies. Four weeks of HFD significantly elevated MAP and visceral adiposity without changing circulating levels of lipids or adipokines. Immunohistochemical analysis demonstrated that SS rats on HFD had significantly greater numbers of CD3+ cells in renal glomerular and medullary areas compared to ND SS rats. Additionally, HFD led to increased glomerular injury, but did not alter renal medullary injury. Chronic MMF treatment in HFD-fed Dahl SS rats reduced MAP, visceral adiposity, infiltration of CD3+ cells in the glomerulus, as well as glomerular injury. However, MMF treatment did not alter HFD-induced infiltration of CD3+ cells in the renal medulla. In conclusion, Dahl SS rats are sensitized to HFD-induced hypertension and renal glomerular injury via infiltration of T lymphocytes.
Highlights
IntroductionHuman studies have suggested a genetic component in the blood pressure responsiveness to increased dietary salt and weight gain (Grim et al 1980; Egan et al 1989; Weinberger 1996; Agapitov et al 2008)
The two major diet-related lifestyle modifications recommended by the American Heart Association to lower blood pressure are reduced salt intake and weight loss (Appel et al 2011).Human studies have suggested a genetic component in the blood pressure responsiveness to increased dietary salt and weight gain (Grim et al 1980; Egan et al 1989; Weinberger 1996; Agapitov et al 2008)
Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society
Summary
Human studies have suggested a genetic component in the blood pressure responsiveness to increased dietary salt and weight gain (Grim et al 1980; Egan et al 1989; Weinberger 1996; Agapitov et al 2008). Previous reports suggest that patients with salt-sensitive (SS) hypertension have a greater blood pressure response to weight gain Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. The Centers for Disease Control and Prevention reported that hypertensive renal injury is not declining and is the ninth cause of death in the United States (Molony and Craig 2009)
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