Microparticles (MPs) are membrane vesicles released during cell activation or apoptosis. Elevated levels of circulating MPs have been detected in pathological states associated with vascular dysfunction. The present study was designed to characterise MPs from both septic shock and healthy subjects and to investigate their effects on vascular functions. MPs were obtained from whole blood of patients (n = 32) or healthy (n = 16) subjects by serial centrifugations. Then, their counts and cellular origins are determined by flow cytometry in platelet-free plasma. Markers of endothelial (CD146), platelet (CD41 and P-selectin: CD62P), and leukocyte (L-selectin: CD62L) activation were measured. Nitric oxide (NO) and superoxide anion (O2-) were measured by electronic paramagnetic resonance technique (ERP). MPs either from patients or healthy subject were injected i.v to mice and then, vascular reactivity was assessed in aorta by myography. Circulating levels of MPs, endothelial- and platelet-derived MPs, as well as P-selectin+ and L-selectin+ MPs were increased in septic patients. No difference in NO or O2- production was detected in mouse aortas treated with MPs from either septic or healthy subjects. MPs either from patients or healthy subjects were injected i.v to mice and then, vascular reactivity was assessed in aorta. Interestingly, the sensitivity of contraction in response to serotonin was increased in aorta taken from mouse treated with septic MPs compared to those with healthy MPs. This effect was not modified in presence either of NO-synthase inhibitor, LNA, or cyclooxygenase (COX)-2 inhibitor, NS398. In other hand, the non-selective COX inhibitor, indomethacin, either reduced or abolished contraction to serotonin in aorta from mice treated with healthy and septic MPs, respectively. Contraction to CaCl2 on arteries exposed to KCl-depolarization and relaxation to the Rho-kinase inhibitor on pre-contracted vessels were identical in aorta taken either from healthy or septic MPs-treated mice. In conclusion, we demonstrate that septic patients displayed increased circulating of MPs especially those originated from non activated and activated platelet, endothelial and activated leucocytes. Interestingly, septic MPs in vivo enhanced reactivity to serotonin without affecting nitrosative or oxidative stresses within the aorta. Thus, septic MPs may be rather protective against vascular hyporeactivity accounting for hypotension in septic shock patients.