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(Circulation Research. 1996;78:424-430.)
© 1996 American Heart Association, Inc.

Articles

cGMP Formation in Rat Atrial Slices Is Ligand and Endothelin Receptor Subtype Specific

Zurit Shraga-Levine, Mordechai Sokolovsky

From the Laboratory of Neurobiochemistry, The George S. Wise Faculty of Life Sciences, Tel Aviv (Israel) University.

Correspondence to Dr Mordechai Sokolovsky, Laboratory of Neurobiochemistry, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel. E-mail sokol@post.tau.ac.il.

Abstract Involvement of a cGMP pathway in signal transduction stimulated by endothelins (ETs) and sarafotoxins (SRTXs) was examined in rat atrial slices. These peptides activated different receptor-binding sites (ET-1 and SRTX-b reacted with the picomolar binding sites of the ET_A receptor, and ET-3 and SRTX-c reacted with the nanomolar binding sites of the ET_B receptor) to produce cGMP. ET-1 and SRTX-b stimulated an increase in cGMP levels via a Ca²⁺-dependent NO pathway involving a pertussis toxin–insensitive G protein, whereas ET-3 and SRTX-c elevated cGMP levels via a Ca²⁺-independent CO pathway involving a pertussis toxin–sensitive G protein. These results can best be explained in terms of formation of different ligand-receptor–G-protein complexes. The ligands had no effect on ventricular slices, indicating that these signal transduction mechanisms are unique to the atria.

Key Words: endothelins • sarafotoxins • rat atria • signaling • cGMP

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