Kishi K, Inoue T
Department of Pharmacology, Jichi Medical School, Tochigi-ken, Japan.
Am J Hypertens. 1990 Aug;3(8 Pt 2):202S-205S. doi: 10.1093/ajh/3.8.202.
This study examined structural and functional changes of mesenteric resistance vessels in early, developing, and established stages of hypertension development in spontaneously hypertensive rats in an attempt to identify possible mechanisms of the development and maintenance of hypertension. Our results suggest that the development of hypertension in spontaneously hypertensive rats may be caused by genetic structural and functional abnormalities of resistance vessels. Both abnormalities may be caused by hyperreactivity to norepinephrine through an altered signal transduction process, including the regulation of protein kinase C in smooth muscle cells of resistance vessels in spontaneously hypertensive rats.
本研究检测了自发性高血压大鼠在高血压发展的早期、发展期和确立期肠系膜阻力血管的结构和功能变化，试图确定高血压发生和维持的可能机制。我们的结果表明，自发性高血压大鼠高血压的发生可能是由阻力血管的遗传性结构和功能异常所致。这两种异常可能是由于对去甲肾上腺素反应过度，通过改变信号转导过程引起的，包括自发性高血压大鼠阻力血管平滑肌细胞中蛋白激酶C的调节。
