Bradykinin does not contribute to hypotension in early canine endotoxemia.

Previous work in this and other laboratories has demonstrated that captopril exacerbates the hypotension produced in dogs by endotoxin. This depressor effect of captopril could result from the potentiation of bradykinin (BK) or inhibited formation of angiotensin II (AII). Anesthetized adult mongrel dogs were used in the current study. In each, the right femoral vein and artery were cannulated for the administration of drugs and monitoring of arterial pressure. A tracheostomy was performed, and the animal was respired with room air. It was found that after injection of endotoxin, AII receptor blockade (Sar1, Ile8-AII) produced a mean arterial pressure (MAP) response statistically similar to that elicited by captopril in combination with endotoxin. Although these results indicate no production of BK, the possibility of BK receptor inactivation during endotoxin shock cannot be disregarded. Additional studies suggested that in the dog, injections of BK can augment the depression of MAP caused by endotoxin and that this further depression can be prolonged by captopril. On the basis of these results, it can be concluded that in the early phases of canine endotoxin shock, AII plays a significant role in the maintenance of MAP and that BK is not produced in quantities sufficient to lower MAP.