Pulmonary endothelium forms the inner lining of blood vessels, where it interprets the complex mechanical and chemical environment within the circulation and adjusts its behavior to facilitate vascular homeostasis. Although endothelium fulfills many essential functions, including regulation of vascular pressure, circulating cell transmigration, coagulation, and hormone metabolism and/or delivery, a principal role is to form a semi-permeable barrier that limits fluid, solute and macromolecular access to the interstitial space. Physiological properties that govern such permeability characteristics are defined by the Starling equation, which assumes that endothelial cells throughout the circulation are all alike. However, in recent years it has become evident that endothelial cells in pulmonary arteries, capillary and veins are heterogeneous in structure and function. Here, we review evidence for endothelial heterogeneity among these pulmonary vascular segments, and consider the implications for such heterogeneity in lung fluid balance, especially as it relates to the Starling equation.
Table of Contents
Defining the Endothelium
The Pulmonary Circulation as Context
General Properties of Endothelium
Transendothelial Fluid Exchange and the Starling Equation
The Starling Equation, Lung Permeability, and Endothelial Heterogeneity
Revised Starling Principles
Heterogeneity and Other Issues
About the Author(s)Mary I. Townsley
, University of South Alabama
Dr. Mary Townsley is Professor of Physiology and Cell Biology and of Internal Medicine at the University of South Alabama College of Medicine. Dr. Townsley's research has broadly focused on theoretical approaches to assessment of lung injury, mechanisms which regulate the integrity of the alveolar septal barrier in the lung and the pathobiology of pulmonary edema and acute lung injury. In addition, she has had a longstanding interest in the pulmonary vascular response to acute pulmonary venous hypertension and chronic pulmonary venous hypertension in left-sided heart failure. These interests led to her current research focus on the role of the vanilloid transient receptor potential calcium channel TRPV4 in acute lung injury.Troy Stevens
, University of South Alabama
Dr. Troy Stevens is the Lenoire Locke Professor and Chair of the Department of Physiology and Cell Biology, Professor of Internal Medicine, and Director of the Center for Lung Biology at the University of South Alabama College of Medicine. Dr. Stevens' lab investigates basic principles of pulmonary vascular biology, with a special emphasis on endothelium. His lab's work has revealed a remarkable heterogeneity in lung endothelial cell structure and function, especially among arterial, capillary and venule vascular segments. This work on endothelial heterogeneity has been incorporated into important physiological concepts, including how fluid moves through the lung, how inflammatory mediators cause pulmonary edema, and how inflammatory cells are recruited to the airways. As part of this progress, several segment-restricted molecules have been identified, both in vivo and in vitro, and their physiological role(s) identified, providing new translational targets for therapeutic development.