Mechanoreception by the endothelium: mediators and mechanisms of pressure- and flow-induced vascular responses.

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158816
G M Rubanyi, A D Freay, K Kauser, A Johns, D R Harder
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引用次数: 164

Abstract

Mechanoreception, a widely distributed sensory modality, has been shown to be present in certain blood vessels. Changes in physical forces, like sudden increase of transmural pressure or flow velocity (shear stress), trigger changes in blood vessel diameter; the former reduces it while the latter increases vessel caliber. These changes in diameter, which are the result of contraction and relaxation of vascular smooth muscle in the blood vessel media, can serve the purpose of physiological regulation of blood flow (autoregulation) and protection of the intima against damages from high shear forces. The precise location of mechanosensor(s) and the mechanism of mechanoreception and signal transduction are poorly understood. Accumulating evidence suggests that the endothelium may be a site of mechanoreception and that changes in the synthesis/release of endothelium-derived relaxing (EDRF, EDHF, PGI2) and contracting factors (EDCF) result in altered vascular smooth muscle tone and vessel caliber. Increased shear stress stimulates the release of EDRF and PGI2 probably via activation of a K+ channel (inward rectifier) in endothelial cell membrane. Endothelium-dependent vascular contraction evoked by increased transmural pressure may be the result of (1) reduced release of EDRF (canine carotid artery) and (2) stimulation of the release of a still unidentified EDCF(s) (feline cerebral artery). Thus the endothelium can serve as pressure and flow sensor and is capable of transducing changes in mechanical forces into changes of vascular smooth muscle tone by modulating the release of endothelium-derived vasoactive factors. The physiological importance of the mechanoreception by endothelial cells in the intact circulation remains to be determined.

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内皮细胞的机械接受:压力和血流诱导的血管反应的介质和机制。
机械感受是一种广泛分布的感觉方式,已被证明存在于某些血管中。物理力的变化,如跨壁压力或流速(剪切应力)的突然增加,引发血管直径的变化;前者减小了压力,后者增大了容器口径。这些直径的变化是血管介质中血管平滑肌收缩和松弛的结果,可以达到血液流动的生理调节(自动调节)和保护内膜免受高剪切力损伤的目的。机械传感器的精确位置以及机械接收和信号转导的机制尚不清楚。越来越多的证据表明,内皮可能是机械接受的一个部位,内皮源性舒张因子(EDRF, EDHF, PGI2)和收缩因子(EDCF)的合成/释放的变化导致血管平滑肌张力和血管直径的改变。增加的剪切应力刺激EDRF和PGI2的释放可能是通过激活内皮细胞膜上的K+通道(向内整流)。经壁压力增加引起的内皮依赖性血管收缩可能是(1)犬颈动脉EDRF释放减少和(2)刺激尚未识别的猫脑动脉EDCF释放的结果。因此,内皮可以作为压力和流量传感器,并能够通过调节内皮源性血管活性因子的释放,将机械力的变化转化为血管平滑肌张力的变化。内皮细胞在完整循环中机械接受的生理重要性仍有待确定。
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