高血压大鼠主动脉对酪氨酸磷酸化抑制剂诱导的血管舒张反应性降低。

Decreased sensitivity of aorta from hypertensive rats to vasorelaxation by tyrphostin.

作者信息

Sauro M D, Thomas B

机构信息

Department of Immunology and Molecular Biology, Masonic Medical Research Laboratory, Utica, NY 13501.

出版信息

Life Sci. 1993;53(22):PL371-6. doi: 10.1016/0024-3205(93)90212-l.

DOI:10.1016/0024-3205(93)90212-l

PMID:8231645

Abstract

The role of protein tyrosine kinases (PTKs) in vascular smooth muscle (VSM) contraction was examined in spontaneously hypertensive rats (SHRs). Aorta from SHRs was hyperresponsive to PTK-mediated contraction relative to normotensive Wistar-Kyoto rats (WKYs). Aorta from SHR was also hyporesponsive to vasorelaxation by tyrphostin, a selective inhibitor of PTKs. Further, we found alterations in PTK activity in aorta from SHRs. PDGF stimulated PTK activity to a greater extent in the SHR. Tyrphostin inhibited PDGF-induced PTK stimulation in both strains, however, activity returned to basal levels in the WKY only. The results suggest that PTKs may be involved in VSM contraction and in the development of hypertension.

摘要

在自发性高血压大鼠（SHR）中研究了蛋白酪氨酸激酶（PTK）在血管平滑肌（VSM）收缩中的作用。相对于血压正常的Wistar-Kyoto大鼠（WKY），SHR的主动脉对PTK介导的收缩反应过度。SHR的主动脉对PTK的选择性抑制剂 tyrphostin引起的血管舒张反应也减弱。此外，我们发现SHR主动脉中PTK活性发生了改变。血小板衍生生长因子（PDGF）在SHR中对PTK活性的刺激作用更大。Tyrphostin在两种品系中均抑制PDGF诱导的PTK刺激，但只有WKY的活性恢复到基础水平。结果表明，PTK可能参与VSM收缩和高血压的发生发展。