Density-dependent contraction of the endothelial nascent histamine pool by exogenous heparin.
The aortic endothelial cell nascent histamine pool has been implicated in the control of vessel wall permeability under conditions of stress and injury. We report the contraction of this histamine pool in low density bovine aortic endothelial cell (BAEC) cultures by exogenous heparin. Untreated BAEC exhibit a decline in histamine content in 3-day cultures with increasing plating density between 1000 and 16,000 cells/cm2. Heparin abolished this density-related difference by effecting a 67% contraction of the histamine pool in the lowest density cultures. This effect was reversible and specific to heparin. At a confluent density, endothelial cells secrete heparin-like glycosaminoglycans which affect smooth muscle and endothelial metabolism. We propose that the metabolic effects of exogenous heparin, and perhaps endogenous heparins, extend to specific modulations of the BAEC nascent histamine pool.
D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000378:metabolism*; D002417:Cattle; D002452:Cell Count; D002809:Chondroitin Sulfates / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004727:Endothelium / Q000378:metabolism; D005260:Female; D006493:Heparin / Q000494:pharmacology*; D006632:Histamine / Q000378:metabolism*; D006640:Histidine Decarboxylase / Q000378:metabolism; D006820:Hyaluronic Acid / Q000494:pharmacology; D011479:Protamines / Q000494:pharmacology
D011479:Protamines; D006632:Histamine; D006820:Hyaluronic Acid; D006493:Heparin; D002809:Chondroitin Sulfates; D006640:Histidine Decarboxylase