Vascular responsiveness to the products of platelet aggregation

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Platelets have been known to produce a labile but potent vasoactive substance as well as to release ADP, ATP and serotonin (5-HT) on stimulation. This substance reported as rabbit aorta contracting substance (RCS) by Piper and Vane2 has been identified as mixture of prostaglandin (PG) endoperoxides (PGG2, PGH2) and thromboxane A2.3 We have reported that; 1) intravascular platelet aggregation induced by ADP produced profound constriction and resultant injury of the pulmonary artery in rabbits; 2) intravenous injection of ADP elicited significantly attenuated cardiorespiratory disturbance and thrombus formation in spontaneously hypertensive rats (SHR) as compared with normal Wistar rats. In this paper in vitro responsiveness of the pulmonary artery of rabbit and the aorta of SHR and vitamine E deficient rat (VEDR) to RCS and 5-HT was investigated.Materials and Methods: 1) The right or left pulmonary artery and thoracic aorta of 9 rabbits, 2) thoracic aorta of 7 pairs of 24-26 weeks old SHR and NWR and 6 pairs of 6 weeks old SHR and NWR, and 3) thoracic aorta of 3 pairs of 11 weeks old VEDR and NWR were excised promptly after death. Each vessels were cut spirally to produce 35-40×2.5-3.0mm strips and the strips were suspended in gassed Krebs medium at 37°C. RCS was generated by agitation of washed rabbit platelets with 5 units of thrombin or 6.25μg of sodium arachidonate for 40sec at 37°C.Results: 1) The contractile response of pulmonary artery to RCS was about 50% of the maximum tension developed by 40mM K+ and 1μM 5-HT. The pulmonary artery response to RCS was as twice greater as the aorta and one to 5-HT was 1.5 times greater (Fig. 1A, B). 2) The contraction of 24-week SHR aorta by RCS was not different from NWR but one by 5-HT was significantly increased. However, the contraction of 6-week SHR aorta was not different from NWR (Fig. 2A, B). 3) Aorta responsiveness of VEDR was not different from NWR (Fig. 3).Comment: Rabbit pulmonary artery contracted in great extent by RCS as well as by 5-HT. Vascular responsiveness of SHR was almost same to NWR or rather increased. So the mechanism of attenuated cardiorespiratory disturbance by intravascular platelet aggregation in SHR may not be on the vessels but on the platelet. Vascular responsiveness of VEDR will be further studied in connection with PGI2.