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Atrial Natriuretic Peptide, a Regulator of Nuclear Factor-B Activation in Vivo

Department of Pharmacy, Center of Drug Research (K.L.-B., M.K., E.K., S.Z., A.M.V.), University of Munich, 81377 Munich, Germany; Department of Pharmacy (A.K.K.), Saarland University, 66041 Saarbrücken, Germany; and Biochemical Pharmacology (A.W.), University of Konstanz, 78457 Konstanz, Germany

Address all correspondence and requests for reprints to: Angelika M. Vollmar, Ph.D., Department of Pharmacy, Center of Drug Research, Butenandtstrasse 5-13, D-81377 Munich, Germany. E-mail: Angelika.Vollmar{at}cup.uni-muenchen.de.

Natriuretic peptides (NPs) comprise a family of vasoactive hormones that play important roles in the regulation of cardiovascular and renal homeostasis. Along this line, atrial NP (ANP) (international non-proprietary name: carperitide, HANP) is an approved drug for the treatment of acute heart failure. In recent years, evidence has been given that the NP system possesses a far broader biological spectrum than the regulation of blood pressure and volume homeostasis. In fact, a substantial amount of in vitro work indicates that ANP affects important inflammatory processes and signaling pathways. Quite surprisingly, however, no information exists on the in vivo antiinflammatory potential and signaling of ANP. We show here that pretreatment of lipopolysaccharide (Salmonella abortus equi, 2.5 mg/kg)-challenged mice with ANP (5 µg/kg iv, 15 min) rapidly inhibits nuclear factor-B activation via inhibition of phosphorylation and degradation of the IB- protein. ANP also reduces Akt activation upon lipopolysaccharide injection. In ANP-pretreated mice, the increase of TNF- serum concentration is markedly prevented; most importantly, the survival of these animals improved. These findings demonstrate both in vitro and in vivo an antiinflammatory profile of ANP that deserves to be further investigated in a therapeutic perspective.

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