1 The induction of B 1 receptors (B 1 Rs) and desensitization or down-regulation of B 2 receptors (B 2 Rs) as a consequence of the production of endogenous kinins has been termed the autoregulation hypothesis. The latter was investigated using two models based on the rabbit: kinin stimulation of cultured vascular smooth muscle cells (SMCs) and in vivo contact system activation (dextran sulphate intravenous injection, 2 mg kg -BK binding or mRNA concentration evaluated by RT ± PCR; 4 or 3 h, respectively). Treatment with B 1 R or B 2 R agonists failed to alter B 1 R expression under the same conditions. 3 Despite consuming endogenous kininogen (assessed using the kinetics of immunoreactive kinin formation in the plasma exposed to glass beads ex vivo) and producing hypotension mediated by B 2 Rs in anaesthetized rabbits, dextran sulphate treatment failed to induce B 1 Rs in conscious animals (RT ± PCR in several organs, aortic contractility). By contrast, lipopolysaccharide (LPS, 50 mg kg 71 , 5 h) was an eective B 1 R inducer (kidney, duodenum, aorta) but did not reduce kininogen reserve. 4 We tested the alternate hypothesis that endogenous kinin participate in LPS induction of B 1 Rs. Kinin receptor antagonists (icatibant combined to B-9858, 50 mg kg 71 of each) failed to prevent or reduce the eect of LPS on B 1 R expression. Dextran sulphate or LPS treatments did not persistently down-regulate vascular B 2 Rs (jugular vein contractility assessed ex vivo). 5 The kinin receptor autoregulation hypothesis is not applicable to primary cell cultures derived from a tissue known to express B 1 Rs in a regulated manner (aorta). The activation of the endogenous kallikrein-kinin system is ineective to induce B 1 Rs in vivo in an experimental time frame sucient for B 1 R induction by LPS.