Endothelin-1 from Pulmonary Artery and Micro vessels Acts on Vascular and Airway Smooth Muscle

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Abstract
Summary The conditioned medium (CM) from microvascular and macrovascular endothelial cell (EC) cultures was tested for constrictor activity. Sheep coronary artery rings, under 1 g tension, and sheep tracheal smooth muscle strips, under 2 g tension, were hung in organ baths containing Krebs-Henseleit solution (39 $$C) and were equilibrated with 95% O2 and 5% CO2. Isometric force was measured in response to 80 mM KC1 and constrictor responses to 100% CM were expressed as a percentage of maximum KC1 response. Serum-free CM from confluent microvascular endothelial cells caused a sustained, slow-onset contraction of the coronary rings similar to that obtained with CM from macrovascular ECs. Indomethacin (5 $mUM) added to either the microvascular or macrovascular CM enhanced the constrictor responses by 1.6-and 1.8-fold, respectively, and the constrictor effects of both media were reduced by the calcium antagonist gallopamil (10 nM). CM from macrovascular EC caused a sustained contraction of tracheal strips similar to microvascular CM. In both cases, constriction was preceded by a brief relaxation as noted in vascular smooth muscle. Unconditioned medium had no constrictor activity on either vascular or airway smooth muscle. Microvascular-derived constrictor activity was heat stable. There was a slight loss of activity in the heat-treated CM from the macrovascular cells compared with control CM. Constrictor effects on tracheal smooth muscle were partially reversed by 1 $mUM gallopamil.

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