Lew R A, Baertschi A J
Department of Physiology University of Virginia Medical Center Charlottesville 22908.
Biochem Biophys Res Commun. 1989 Sep 15;163(2):701-9. doi: 10.1016/0006-291x(89)92280-8.
Using a novel in vitro co-culture system, we investigated the possible influence of vascular endothelial cells on the secretion of atrial natriuretic factor (ANF) from atrial myocytes. Co-culture of bovine aortic endothelial cells grown on Cytodex-3 microcarrier beads with primary monolayer cultures of neonatal rat myocytes induced a 2.1-fold increase in immunoreactive ANF (irANF) in the medium, compared with irANF in medium from atrial cultures alone. This increase did not appear to be the result of processing of prohormone to more immunoreactive species, and could be inhibited by 47% with 10 microM acetylcholine. The endothelium-derived vasoconstrictor peptide, endothelin, elicited a dose-dependent increase in ANF secretion from atrial cultures, but, contrary to vasopressin, was incapable of further stimulating release from atrial-endothelial co-cultures. These experiments suggest that endothelium stimulates the release of ANF from myocytes, possibly by the action of the peptide endothelin.
利用一种新型的体外共培养系统，我们研究了血管内皮细胞对心房肌细胞分泌心房利钠因子（ANF）的可能影响。在Cytodex - 3微载体珠上生长的牛主动脉内皮细胞与新生大鼠心肌细胞的原代单层培养物共培养，与仅来自心房培养物的培养基中的免疫反应性ANF（irANF）相比，培养基中的irANF增加了2.1倍。这种增加似乎不是前激素加工成更多免疫反应性物质的结果，并且10 microM乙酰胆碱可抑制47%。内皮源性血管收缩肽内皮素引起心房培养物中ANF分泌的剂量依赖性增加，但与加压素相反，它不能进一步刺激心房 - 内皮共培养物中的释放。这些实验表明，内皮可能通过肽内皮素的作用刺激心肌细胞释放ANF。
