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. 1985 Jul;44(10):2603-9.

The pulmonary endothelial surface

  • PMID: 3891415

The pulmonary endothelial surface

U S Ryan et al. Fed Proc. 1985 Jul.

Abstract

The understanding of endothelial metabolic properties has increased dramatically in recent years. Endothelial cells (ECs) process hormones, drugs, and many blood-borne substances by means of enzymes and transport processes. In turn, some hormones, blood cells, and cellular products interact with ECs via specific receptors on the luminal surface. Functional complexity is exemplified by the metabolism of the adenine nucleotides. ATP, ADP, and AMP are metabolized by enzymes of the endothelial surface to release adenosine, which may be immediately taken up into endothelium and reincorporated intracellularly into nucleotides. Equally complex is the metabolism of the kinins and angiotensins by ECs. Bradykinin is inactivated whereas angiotensin I is converted to angiotensin II. Bradykinin not thus degraded can act on endothelial receptors and stimulate the release of prostacyclin (PGI2). Thus bradykinin can amplify the release of another vasodilator, PGI2, and can stimulate the release of a powerful antiaggregatory agent (PGI2). Many of these complex metabolic reactions occur at the endothelial surface, a structure that is itself complex. ECs possess endothelial projections and caveolae as well as a fuzzy coat, or glycocalyx. Functions of the endothelial glycocalyx are not well understood, but the glycocalyx can now be visualized: it may act as a molecular sieve and provide a substratum for the initiation and progression of immunologic reactions.

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