Coronary microvascular endothelial cells cosecrete angiotensin II and endothelin-1 via a regulated pathway

DOI Web Site 被引用文献1件
  • Yasuko Kusaka
    Division of Cardiology, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachuesetts 02115
  • Ralph A. Kelly
    Division of Cardiology, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachuesetts 02115
  • Gordon H. Williams
    Division of Endocrinology-Hypertension and
  • Imre Kifor
    Division of Endocrinology-Hypertension and

書誌事項

公開日
2000-09-01
DOI
  • 10.1152/ajpheart.2000.279.3.h1087
公開者
American Physiological Society

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説明

<jats:p>Although endothelial cells produce angiotensin II (ANG II) and endothelin-1 (ET-1), it is not clear whether a single cell produces both peptides, with cosecretion in response to stimulation, or whether different subpopulations of endothelial cells secrete one or the other peptide, with secretion in response to different stimuli. Exposure of cultured coronary microvascular endothelial cells to cycloheximide for 60 min had no effect on ANG II or ET-1 secretion. This result suggested the existence of a preformed intracellular pool of ANG II and ET-1, which is a precondition for regulated secretion. Exposure of endothelial cells to isoproterenol, high extracellular potassium, or cadmium, all of which stimulate peptide secretion via different signaling pathways, significantly ( P > 0.001) increased the secretion of both ANG II and ET-1 in a cell size-dependent manner. Sodium nitroprusside and S-nitroso- N-acetyl penicillamine significantly ( P > 0.001) decreased ANG II and ET-1 secretion, whereas N<jats:sup>ω</jats:sup>-nitro-l-arginine-methyl ester enhanced it. The similar regulation of ANG II and ET-1 secretion and the presence of both peptides around individual endothelial cells indicate that the autocrine/paracrine regulation of cardiovascular function by endothelial cells is accomplished via cosecretion of ANG II and ET-1.</jats:p>

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