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Am J Physiol Renal Physiol (November 19, 2002). doi:10.1152/ajprenal.00264.2002
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Articles in PresS, published online ahead of print November 19, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00264.2002
Submitted on July 23, 2002
Accepted on November 2, 2002

MELATONIN REDUCES RENAL INTERSTITIAL INFLAMMATION AND IMPROVES HYPERTENSION IN SPONTANEOUSLY HYPERTENSIVE RATS

Mayerly Nava1, Yasmir Quiroz1, Nosratola D. Vaziri2, and Bernardo Rodriguez-Iturbe1*

1 Division of Nephrology, Hospital Universitario, Universidad del Zulia and Instituto de Investigaciones Biomedicas, Fundacite-Zulia, Maracaibo, Zulia, Venezuela
2 Division of Nephrology and Hypertension, Department of Medicine, Physiology and Biophysics, University of California, Irvine, Irvine, California, USA

* To whom correspondence should be addressed. E-mail: bri{at}iamnet.com.

Several studies have demonstrated that treatment with antioxidants improve hypertension in spontaneously hypertensive rats (SHR). Since we have shown that renal infiltration of immune cells play a role in the development of hypertension, we did the present studies to define if the anti-hypertensive effect of antioxidants was associated with improvement of renal inflammation. Melatonin (MEL) was administered as antioxidant. During 6 weeks, MEL was added to the drinking water (10 mg per 100 ml) given to a group SHR (SHR-MEL, n=10) and compared them with a group of untreated SHR (n=10) and with WKY control rats (n=10). Hypertension became increasingly severe in the SHR group (195±SD14.3 mmHg at the end of the experiment) and improved in the SHR-MEL group (149±20.4 mmHg, p<0.001) in association with a forty to sixty percent reduction in the renal infiltration of lymphocytes, macrophages, and angiotensin II positive cells. Intracellular superoxide and renal malondialdehyde content were reduced by MEL treatment, as also was the immunohistological expression of the 65kDA DNA-binding subunit of NF-{kappa}B. We conclude that MEL treatment ameliorates hypertension in the SHR in association with a reduction in the interstitial renal inflammation. Decreased activation of NF-{kappa}B, likely resulting from a reduction in local oxidative stress, may play a role in the suppression of the renal immune infiltration and, thereby, in the anti-hypertensive effects of MEL.




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