Angiotensin delays platelet aggregation after injury of cerebral arterioles

William I. Rosenblum, Farouk El Sabban, Paul D. Hirsh

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Endothelium of cerebral surface vessels (plal arterioles and venules) was Injured with a light/dye technique in anesthetized mice. This induced platelet aggregation at the site of injury. The onset of agregation was monitored through a microscope in mice given angiotensin II acetate, 4 µg i.v. 30 minutes earlier. Aggregation latency was compared with that in vehicle treated (saline) mice. Angiotensin II caused a highly significant delay in agggregation 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 µM ADP or 0.5 mM sodium arachidonate. Angiotensin is a well known stimulator of prostacyclin synthesis or release, and angiotensin has been reported to inhibit platelet aggregation 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 microvascu-lar 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.

Original languageEnglish
Pages (from-to)1203-1205
Number of pages3
Issue number6
StatePublished - 1986
Externally publishedYes


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