Iida N
Department of Physiology, School of Medicine, University of Hiroshima, Japan.
Hypertension. 1995 Feb;25(2):260-5. doi: 10.1161/01.hyp.25.2.260.
The aims of this study were to elucidate the vasoconstrictor mechanism that mediates the changes in celiac and mesenteric vascular resistances during vasoconstriction and hypertension induced by ganglionic blockade and to explore the preferential mechanism that contributes to the elevation of arterial pressure in conscious spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rats, blood flow and arterial pressure were measured with an implanted electromagnetic flow probe and an indwelling arterial catheter. Peripheral vascular resistance was calculated as arterial pressure divided by regional flow. Celiac contribution to the hypertension in SHR was below average for the entire body and was smaller than that from the superior mesenteric bed. The increase of mesenteric resistance with arterial pressure elevation after ganglionic blockade suggests that mesenteric blood flow is regulated by a stretch-dependent myogenic mechanism, whereas celiac blood flow is regulated preferentially by the sympathetic neural mechanism. It is speculated that the flow superregulation in the mesenteric bed in SHR is due to the enhanced myogenic response and contributes to the early stage of hypertension.
本研究的目的是阐明在神经节阻断诱导的血管收缩和高血压期间介导腹腔和肠系膜血管阻力变化的血管收缩机制，并探索导致清醒自发性高血压大鼠（SHR）动脉血压升高的优先机制。在清醒的SHR和正常血压对照大鼠中，使用植入式电磁流量探头和留置动脉导管测量血流量和动脉血压。外周血管阻力计算为动脉血压除以局部血流量。腹腔对SHR高血压的贡献在全身中低于平均水平，且小于来自肠系膜上血管床的贡献。神经节阻断后肠系膜阻力随动脉血压升高而增加，这表明肠系膜血流量受牵张依赖性肌源性机制调节，而腹腔血流量优先受交感神经机制调节。据推测，SHR肠系膜血管床中的血流超调节是由于肌源性反应增强，并且促成了高血压的早期阶段。
