A possible involvement of endocannabinoids in a chronic model of endotoxemia was assessed by measuring the regional (renal, mesenteric, hindquarters) hemodynamic responses to continuous, 24 h lipopolysaccharide (LPS) infusion (150 µg/kg/h) in conscious, male Sprague-Dawley rats, in the absence or presence of the cannabinoid (CB₁) receptor antagonist, AM 251 (3 mg/kg). AM 251 inhibited the tachycardic and hindquarters vasodilator effects of LPS, but did not influence the other hemodynamic changes. In subsequent experiments it was shown that the tachycardic and hindquarters vasodilator effects of LPS were also inhibited by the non-selective -adrenoceptor antagonist, propranolol. In addition, the late (at 24 h) hindquarters vasodilator effects of LPS were inhibited by the ₂-adrenoceptor antagonist, ICI 118551. Against the background of our previous work showing -adrenoceptor involvement in the cardiovascular effects of exogenous cannabinoids, we conclude that AM 251 may have been inhibiting endocannabinoid-modulated, sympathoadrenal-mediated activation of vasodilator -adrenoceptors in LPS-infused rats, rather than suppressing a direct vasodilator action of endocannabinoids.