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Vol. 25, No. 5, 2002   

Free Abstract     Article (References)     Article (PDF 163 KB)     

Original Paper

Effect of Angiotensin II on ANP-Dependent Guanylyl Cyclase Activity in Cultured Mouse and Rat Podocytes
Magdalena Golosa, Barbara Lewkoa, Ewa Bryla, Jacek M. Witkowskib, Anna Dubaniewiczb, Agnieszka Olszewskaa, Elzdotbieta Latawieca, Stefan Angielskia,c, Jan Stepinskia,c

Departments of
aImmunopathology and
bPathophysiology, Medical University of Gdanacutesk, and
cLaboratory of Cellular and Molecular Nephrology, Medical Research Centre of the Polish Academy of Sciences, Warsaw, Poland

Address of Corresponding Author

Kidney & Blood Pressure Research 2002;25:296-302 (DOI: 10.1159/000066790)


 goto top of page Key Words

  • Podocytes
  • Guanylyl cyclases
  • Angiotensin II
  • Natriuretic peptides

 goto top of page Abstract

The presence of a well-developed contractile apparatus is the feature determining major roles of podocytes in the renal glomeruli. Receptors for a variety of vasoactive hormones are expressed in these cells; however, most of the signaling pathways are still unknown and remain to be elucidated. Angiotensin II (Ang II) and atrial natriuretic peptide (ANP), due to their opposite action, are the major modulators of glomerular filtration. In podocytes, Ang II induces rise in intracellular calcium concentration, whereas ANP stimulates generation of cGMP. The present study was designed to check whether ANP-stimulated cGMP synthesis in podocytes might be affected by Ang II. Cultured rat (RP) and mouse (MP) podocytes were stimulated with ANP, in the absence or presence of Ang II and cyclic GMP was determined by RIA method. Co-incubation of podocytes with ANP and Ang II caused significant (p < 0.01) suppression of ANP-dependent cGMP generation. The effect was prevented by saralasin, an inhibitor of angiotensin receptors. Phorbol-12-myristate-13-acetate (PMA) mimicked, whereas chelerythrine reversed inhibitory effect of Ang II. In conclusion, angiotensin II counteracts ANP-stimulated cGMP synthesis in cultured podocytes. It seems likely that the protein kinase C pathway is involved in this effect.

Copyright © 2002 S. Karger AG, Basel


 goto top of page Author Contacts

Barbara Lewko, PhD
Department of Immunopathology
Medical University of Gdanacutesk, ul. Debinki 7
80-952 Gdanacutesk (Poland)
Tel. +48 58 349 2186, Fax +48 58 349 2191, E-Mail blew@amedec.amg.gda.pl


 goto top of page Article Information

Accepted: July 1, 2002
Number of Figures : 5, Number of Tables : 2, Number of References : 37

 
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