PMID- 12091051 OWN - NLM STAT- MEDLINE DCOM- 20030304 LR - 20190727 IS - 0049-3848 (Print) IS - 0049-3848 (Linking) VI - 105 IP - 6 DP - 2002 Mar 15 TI - There is no valid evidence presented as to an impaired endothelial NO system in the stroke-prone spontaneously hypertensive rats. PG - 507-11 AB - Platelet reactivity in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were compared. In vivo platelet reactivity was tested by the He-Ne laser-induced thrombosis model. The number of laser pulses needed to reach thrombotic occlusion of the targeted vessel was used as an index of thrombogenicity. SHRSP rats needed significantly less number of irradiation to reach occlusion than WKY rats (SHRSP vs. WKY, 5.1+/-0.3 vs. 8.1+/-0.6), indicating enhanced thrombotic response in SHRSP rats. Further, acetylcholine administration significantly increased the number of laser pulses until occlusion in WKY but not in SHRSP rats. This suggests an impaired thrombotic reaction in acetylcholine-treated WKY but not in SHRSP rats. Platelet reactivity in vitro was measured in native blood by a shear-induced haemostasis test (haemostatometry). Indexes of this test (H1/H2), which inversely correlated with platelet reactivity, were significantly greater in SHRSP than in WKY rats (SHRSP vs. WKY, H1: 1815+/-192 vs. 763+/-75; H2: 7547+/-723 vs. 3536+/-264). This suggests reduced platelet reactivity in SHRSP compared with WKY rats. Thus, the present findings show increased thrombotic tendency in SHRSP rats in vivo despite reduced platelet reactivity in vitro. To explain this contradiction, we suggest that an increased in vivo thrombotic tendency may be due to impaired nitric oxide (NO) release from endothelial cells in SHRSP rats, and that a reduced platelet reactivity in vitro may be due to an adaptation of SHRSP rats to survive at extremely high blood pressure. FAU - Yamashita, T AU - Yamashita T AD - Laboratory of Physiology, Faculty of Nutrition and High Technology Research Centre, Kobegakuin University, Arise 518, Igawadani-cho, Kobe 651-2180, Japan. tsutomu@nutr.kobegakuin.ac.jp FAU - Taka, T AU - Taka T FAU - Nojima, R AU - Nojima R FAU - Ohta, Y AU - Ohta Y FAU - Seki, J AU - Seki J FAU - Yamamoto, J AU - Yamamoto J LA - eng PT - Comparative Study PT - Journal Article PL - United States TA - Thromb Res JT - Thrombosis research JID - 0326377 RN - 31C4KY9ESH (Nitric Oxide) RN - N9YNS0M02X (Acetylcholine) SB - IM MH - Acetylcholine/administration & dosage/pharmacology MH - Adaptation, Physiological MH - Animals MH - Disease Models, Animal MH - Endothelium, Vascular/*metabolism MH - Hypertension/etiology MH - Lasers MH - Male MH - Nitric Oxide/*metabolism/pharmacology MH - Platelet Activation MH - Rats MH - Rats, Inbred SHR/*physiology MH - Rats, Inbred WKY MH - Stress, Mechanical MH - Stroke/*etiology MH - Thrombosis/etiology EDAT- 2002/07/02 10:00 MHDA- 2003/03/05 04:00 CRDT- 2002/07/02 10:00 PHST- 2002/07/02 10:00 [pubmed] PHST- 2003/03/05 04:00 [medline] PHST- 2002/07/02 10:00 [entrez] AID - S0049384802000695 [pii] AID - 10.1016/s0049-3848(02)00069-5 [doi] PST - ppublish SO - Thromb Res. 2002 Mar 15;105(6):507-11. doi: 10.1016/s0049-3848(02)00069-5.