Role of extracellular signal-regulated kinases (ERK) in leptin-induced hypertension

Life Sciences
Grazyna WójcickaJerzy Bełtowski

Abstract

We investigated if extracellular signal-regulated kinases (ERK) and oxidative stress are involved in the pathogenesis of arterial hypertension induced by chronic leptin administration in the rat. Leptin was administered at a dose of 0.25 mg/kg twice daily s.c. for 4 or 8 days. Blood pressure (BP) was higher in leptin-treated than in control animals from the third day of the experiment. The superoxide dismutase (SOD) mimetic, tempol, normalized BP in leptin-treated rats on days 6, 7 and 8, whereas the ERK inhibitor, PD98059, exerted a hypotensive effect on days 3 through 6. Leptin increased ERK phosphorylation level in renal and aortic tissues more markedly after 4 than after 8 days of treatment. In addition, leptin reduced urinary Na(+) excretion and increased renal Na(+),K(+)-ATPase activity, and these effects were abolished on days 4 and 8 by PD98059 and tempol, respectively. The levels of NO metabolites and cGMP were reduced in animals receiving leptin for 8 days. Markers of oxidative stress (H(2)O(2) and lipid peroxidation products) were elevated to a greater extent after 4 than after 8 days of leptin treatment. In contrast, nitrotyrosine, a marker of protein nitration by peroxynitrite, was higher in animals receiving lepti...Continue Reading

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Citations

Jan 5, 2011·Antioxidants & Redox Signaling·Maurizio Parola, Fabio Marra
Nov 26, 2008·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Samuele De MinicisDavid A Brenner
May 23, 2012·Archives of Oral Biology·Daisuke EkuniManabu Morita
Jan 20, 2018·Journal of Cellular Physiology·Jin XuLanfang Li
Dec 5, 2017·Experimental and Therapeutic Medicine·Yuelin ChenJun Li
Aug 12, 2008·Molecular and Cellular Biochemistry·Jerzy BełtowskiAndrzej Wojtak

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