Abstract
Cardiovascular effects of hog pancreatic kallikrein were investigated in comparison with those of kallidin in anesthetized, open-chest dogs and canine heart-lung preparations. Systemically intravenous injections of kallikrein (0.01 ?? 0.1unit/kg) to anesthetized intact dogs markedly increased regional blood flows in the following order: vertebral>femoral>intracarotid>corcnary>anterior mesenteric>renal arteries. Intraarterial injections of kallikrein (0.01 ?? 0.1 unit) and kallidin (0.3 ?? 3.0 ng) produced a similar, dose-dependent increase in blood flows in the above vascular beds. The effect on the femoral arterial bed was most remarkable. The order of the responses among the other vascular regions was the same as seen in cases of intravenous administration of kallikrein. Systemically intravenous or close intraportal injections of kallikrein and kallidin produced a negligible effect on portal blood flow. In open-chest dogs, kallikrein given intravenously and into the left atrium produced hypotension, an increase in cardiac output and a decrease in left ventricular pressure, without any accompanying changes in cardiac contractile force. On the contrary, no effect was observed on cardiac output, heart rate and right atrial pressure following administration of kallikrein in canine heart-lung preparations. Intraarterial or intra-left atrial injections of kallidin produced almost the same cardiovascular effects as did those of kallikrein in the above preparations, whereas kallidin given intravenously or into the right atrium had no effect. From the above findings it is indicated that kallikrein increases blood flow particularly in cerebral, femoral and coronary vasculatures, has no direct inotropic and chronotropic effect, and in contrast with kallidin is inactivated little in the lung.
