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Am J Physiol Renal Physiol 276: F433-F441, 1999;
0363-6127/99 $5.00
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Vol. 276, Issue 3, F433-F441, March 1999

AVP inhibits LPS- and IL-1beta -stimulated NO and cGMP via V1 receptor in cultured rat mesangial cells

Tetsuo Umino1, Eiji Kusano1, Shigeaki Muto1, Tetsu Akimoto1, Satoru Yanagiba1, Shuichi Ono1, Morimasa Amemiya1, Yasuhiro Ando1, Sumiko Homma1, Uichi Ikeda2, Kazuyuki Shimada2, and Yasushi Asano1

Departments of 1 Nephrology and 2 Cardiology, Jichi Medical School, Tochigi, 329-0498 Japan

The present study examined how arginine vasopressin (AVP) affects nitric oxide (NO) metabolism in cultured rat glomerular mesangial cells (GMC). GMC were incubated with test agents and nitrite, and intracellular cGMP content, inducible nitric oxide synthase (iNOS) mRNA, and iNOS protein were analyzed by the Griess method, enzyme immunoassay, and Northern and Western blotting, respectively. AVP inhibited lipopolysaccharide (LPS)- and interleukin-1beta (IL-1beta )-induced nitrite production in a dose- and time-dependent manner, with concomitant changes in cGMP content, iNOS mRNA, and iNOS protein. This inhibition by AVP was reversed by V1- but not by oxytocin-receptor antagonist. Inhibition by AVP was also reproduced on LPS and interferon-gamma (IFN-gamma ). Protein kinase C (PKC) inhibitors reversed AVP inhibition, whereas PKC activator inhibited nitrite production. Although dexamethasone and pyrrolidinedithiocarbamate (PDTC), inhibitors of nuclear factor-kappa B, inhibited nitrite production, further inhibition by AVP was not observed. AVP did not show further inhibition of nitrite production with actinomycin D, an inhibitor of transcription, or cycloheximide, an inhibitor of protein synthesis. In conclusion, AVP inhibits LPS- and IL-1beta -induced NO production through a V1 receptor. The inhibitory action of AVP involves both the activation of PKC and the transcription of iNOS mRNA in cultured rat GMC.

nitrite production; oxytocin receptor; inducible nitric oxide synthase; V1-receptor antagonist; oxytocin receptor antagonist; lipopolysaccharide


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