Mechanisms of ex vivo aortic hypocontractility in endotoxemic rat.

To clarify the mechanism of the vascular hypocontractility in endotoxemia, the effect of endotoxin injection on phosphatidylinositol turnover and the contractile responses to NH4Cl and okadaic acid were investigated in aorta dissected from rats. The basal level of phosphatidylinositol hydrolysis and the phenylephrine- and 5-hydroxytryptamine-stimulated increase in hydrolysis were all markedly reduced in endotoxemic aortas as compared to in control aortas. Stimulation with KCl did not increase phosphatidylinositol hydrolysis in control or endotoxemic aortas. The NH4Cl-induced contractile response was significantly diminished in endotoxemic aorta, whereas the okadaic acid-induced contractile response was not altered. These results suggest that both transmembrane and intracellular signal transduction mechanisms are impaired in the endotoxemic artery whereas the contractile machinery remains intact.