Endothelial contractility - an undecided problem in vascular research.
The rather old conception that endothelial cells possess an autonomous contractile capability has been reevaluated by several suthors during the past ten years on the basis of three different arguments of various validity: (1) After the topical application of inflammatory mediators tmajno et al. regularly found the endothelial nuclei furnished with numerous identations together with many interendothelial "gaps"; Both findings are assumed to be the morphological correlate of an endothelial shortening due to the contraction of the cells. While nuclear indentations seemed to be a rather weak argument to substantiate contractile capabilities, a mechanism other than contraction is outlined for the formation of "gaps"; (2) The second argument in favour of endothelial contractility is the occurrence of cytoplasmic filaments that occasionally form cross striated bundles and/or show a "thick" and "thin" variety. If all these data are assumed to be the morphological evidence for the contractile capability of cells then the conclusion: the more filaments the higher the contractile activity, must be valid. But when compiling those endothelia that are particularly rich in filaments this conclusion does not make sense, because e.g. the endothelium covering the venous valves is crowded with filaments yet an especially high "contractile activity" does not seem very probabble. On the other hand, the supposition that endothelial conttractility is entirely independent of the existence of cytoplasmic filaments leaves the question unanswered what then are the filaments for if not serving mechanical purposes. This line of reasoning is supported by both the localization of the filaments predominantly in those endothelia that have to sustain higher degrees of various mechanical stresses and the fact that filamentous structures significatnly increase in number under the influence of hypertension. (3) The final argument brought forward to substantiate endothelial contractility is the demonstration of actin and tropomyosin in the endothelium of various types of blood vessels that also occur under the influence of hypertension; tbut the significance of these findings as a proof for endothelial contractility is curtailed by the fact that the occurrence of actin alone is not conclusive for any contractile capabilities; Furthermore, a convincing demonstration of myosin in endothelial cells is still lacking and the "thick" filaments are believed to be noncontractile. Hence we suggest that the endothelial filaments together with the myoid proteins do not serve as a means for "contractility" in a true sense but simply act as a design to originate tensile strength.
D000818:Animals; D001808:Blood Vessels / Q000502:physiology* / Q000648:ultrastructure; D002467:Cell Nucleus / Q000648:ultrastructure; D003250:Constriction; D004727:Endothelium / Q000502:physiology / Q000648:ultrastructure; D006801:Humans; D002479:Inclusion Bodies / Q000648:ultrastructure; D007365:Intercellular Junctions / Q000648:ultrastructure; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000032:analysis; D009130:Muscle, Smooth / Q000502:physiology
D009124:Muscle Proteins