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Endothelial contractility an undecided problem in vascular research



Endothelial contractility an undecided problem in vascular research



Beitraege zur Pathologie 157(4): 327-348



The rather old concept that endothelial cells possess autonomous contractility was reevaluated by several authors during the past 10 yr on the basis of 3 different arguments of various validity. After the topical application of inflammatory mediators Majno et al. regularly found endothelial nuclei with numerous indentations and many interendothelial gaps. Both findings are assumed to be morphological correlates 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. The 2nd argument in favor of endothelial contractility is the occurrence of cytoplasmic filaments that occasionally form cross striated bundles and/or show a thick and thin variety. If these data are assumed to be morphological evidence for the contractility of cells then the conclusion that the more filaments the higher the contractile activity, must be valid. But when compiling those endothelia particularly rich in filaments this conclusion does not seem valid, because, e.g., the endothelium covering the venous valves is crowded with filaments yet an especially high contractile activity does not seem very probable. Conversely, the supposition that endothelial contractility 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 localization of the filaments predominantly in those endothelia that have to sustain higher degrees of various mechanical stresses and the fact that these filamentous structures significantly increase in number under the influence of hypertension. 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. 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. A convincing demonstration of myosin in endothelial cells is still lacking and the thick filaments are believed to be noncontractile. The endothelial filaments together with the myoid proteins may not serve as a means for contractility in a true sense but simply act as a design to originate tensile strength.

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Accession: 005359985

Download citation: RISBibTeXText

PMID: 183655

DOI: 10.1016/s0005-8165(76)80049-2



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