Rubanyi G M, Freay A D, Kauser K, Johns A, Harder D R
Department of Pharmacology, Berlex Laboratories, Cedar Knolls, N.J.
Blood Vessels. 1990;27(2-5):246-57. doi: 10.1159/000158816.
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.
机械感受是一种广泛分布的感觉模式，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，会引发血管直径的变化；前者使其减小，而后者则增加血管口径。这些直径的变化是血管中膜血管平滑肌收缩和舒张的结果，可用于生理调节血流（自身调节）以及保护内膜免受高剪切力的损伤。机械感受器的确切位置以及机械感受和信号转导的机制尚不清楚。越来越多的证据表明，内皮可能是机械感受的部位，内皮衍生的舒张因子（内皮舒张因子、内皮超极化因子、前列环素）和收缩因子（内皮收缩因子）合成/释放的变化会导致血管平滑肌张力和血管口径改变。增加的剪切应力可能通过激活内皮细胞膜上的钾通道（内向整流器）刺激内皮舒张因子和前列环素的释放。跨壁压力增加引起的内皮依赖性血管收缩可能是以下结果：（1）内皮舒张因子释放减少（犬颈动脉）和（2）刺激释放一种尚未确定的内皮收缩因子（猫脑动脉）。因此，内皮可作为压力和流量传感器，并能够通过调节内皮衍生的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的机械感受的生理重要性仍有待确定。
