The ability of an arteriole to conduct vasomotor responses along its length contributes to the control of organ perfusion. Sepsis, a systemic inflammatory response to infection, may compromise this control. We aimed to determine whether sepsis, induced by cecal ligation and perforation (CLP), reduces conducted vasoconstriction 24 h post-CLP. We locally stimulated mouse cremaster arterioles with KCl, measured the resulting local and the conducted constriction (500 µm upstream) and, based on these measurements, determined the communication ratio (CR<sub>500</sub>) as an index of the conducted response. Sepsis significantly reduced the CR<sub>500</sub> from 0.75 to 0.20. Based on a mathematical model, this reduction was predicted to have a significant impact on blood flow control. In septic mice, either a 1-hour washout of the cremaster muscle with physiological saline or a treatment of this muscle with the tyrosine kinase inhibitor PP-2 (100 n M) restored the CR<sub>500</sub> to the control level. Treatment of septic arterioles with the nitric oxide synthase inhibitor N<sup>ω</sup>-nitro- L-arginine methyl ester (100 µ M) partially restored the CR<sub>500</sub> from 0.2 to 0.4. In control mice, lipopolysaccharide (LPS; 10 µg/ml) superfused over the cremaster muscle for 1 h reduced the CR<sub>500</sub>; the nitric oxide (NO) donor S-nitroso-N-acetyl-penicillamine (50 µ M) also reduced the CR<sub>500</sub>. Thus, LPS and NO could be two factors mediating reduced conduction of vasoconstriction in sepsis. We conclude that sepsis reduces the KCl-induced conducted vasoconstriction in the mouse cremaster muscle by a tyrosine kinase- and nitric oxide- dependent mechanism.