Shear stress activates ISAC (non-selective current) and reduces IK1. Since concomitant Na accumulation is measured also outside the stretched area, signals of SMIC may spread out by means of a diffusible second messenger (NO during stretch: Petroff et al., 2000). Efficacy of SMIC was reduced by quenching NO with TPIO, by reducing NO synthesis with LNMMA, or in cells from eNOS -/-mice. SMIC was also blocked by quenching *O_{2- with Tiron or} by inhibition of NADPH oxidase (NOX) with apamycin or DPI. Presumably, both eNOS and NOX are stretch sensitive. Wesuggest that ^*O2- can oxidize *NO to ONOO (Peroxinitrit) whose life time long is enough for a second messenger function. Albumin blocked SICM as if cationic fatty acids (FA) would contribute to signalling cascade of SMIC (Petrou et al., 1995). Application of FA mimicked SMIC, these signals persisted when ONOO formation was blocked. We hypothesize: the messenger ONOO activates a phospholipase that increases the amount of CoA-FA known to compete with PIP_{2 at the cytosolic side of}channel proteins. Accordingly, SMIC were obtained by application of poly-L-lysine to the cytosol shielding charges of PIP_2.