INTERACTION OF ISATIN WITH TYPE-A NATRIURETIC PEPTIDE RECEPTOR - POSSIBLE MECHANISM

The effect of isatin on rat brain particulate guanylate cyclase (GC) w as investigated. The enzyme was stimulated by atrial natriuretic pepti de (ANP), brain natriuretic peptide (BNP) and urodilatin, but not by C -type natriuretic peptide (CNP). Their effects were not additive, poin ting to action via the GC-A receptor. Isatin, in dose-dependent manner , abolished this stimulation. The non-hydrolysable ATP analogue, adeny lylimidodiphosphate, potentiated the effects of submaximal doses of AN P, BNP and urodilatin on this particulate GC-A, and attenuated or abol ished sensitivity to isatin. These results suggest that isatin antagon ises the generation of second messenger by GC-A; this sensitivity migh t be regulated at an ATP binding site, possibly a protein kinase-like domain.