Angiotensin delays XXXX after injury of cerebral arterioles.

@entity1423 @entity19 @entity7774 @entity598 @entity1426 @entity857
Endothelium of cerebral surface vessels (pial arterioles and venules) was injured with a light/dye technique in anesthetized @entity19 . This induced @entity1423 at the site of injury. The onset of aggregation was monitored through a microscope in @entity19 given angiotensin II @entity598 , 4 micrograms i.v. 30 minutes earlier. Aggregation latency was compared with that in vehicle treated (saline) @entity19 . Angiotensin II caused a highly significant delay in aggregation within the arterioles which was not related to a change in shear rate of blood. Angiotensin II added to platelet rich plasma, failed to influence the aggregation produced by subsequent addition of 0.5 microM @entity857 or 0.5 mM @entity1426 . @entity7774 is a well known stimulator of prostacyclin synthesis or release, and @entity7774 has been reported to inhibit @entity1423 ex vivo by increasing prostacyclin in the effluent superfusing the mass of aggregating platelets. Our data represent the first report of an antiaggregating effect of angiotensin II in vivo in an intact microvascular bed. The data is consonant with the literature describing increased prostacyclin levels following angiotensin II infusion. The antiaggregating effect of angiotensin in cerebral microvessels may help explain a recent observation describing increased survival of gerbils treated with angiotensin following carotid ligation.
