These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Calcium influx into endothelial cells and formation of endothelium-derived relaxing factor is controlled by the membrane potential.
    Author: Lückhoff A, Busse R.
    Journal: Pflugers Arch; 1990 May; 416(3):305-11. PubMed ID: 2381766.
    Abstract:
    We studied the role of the membrane potential in the control of the intracellular free calcium concentration ([Ca2+]i) and release of the two autacoids endothelium-derived relaxing factor (EDRF = nitric oxide) and prostaglandin I2 in endothelial cells. ATP (3 mumol/l) and bradykinin (1 nmol/l) evoked rapid increases (sixfold) in [Ca2+]i in cultured endothelial cells. [Ca2+]i remained elevated over several minutes. When the cells were depolarized, either by K+ (70-90 mmol/l) or by preincubation with the blocker of K+ channels tetraethylammonium (3 mmol/l), the initial peak of [Ca2+]i remained unaffected but [Ca2+]i returned significantly faster to resting levels, indicating a reduction in Ca2+ influx. In native, freshly isolated endothelial cells, K+ abolished increases in [Ca2+]i induced by acetylcholine (3 mumol/l). Release of EDRF in response to bradykinin (cultured cells) and acetylcholine (native cells) was inhibited by K+ (by 70%), whereas release of prostaglandin I2 was not significantly reduced. Preincubation of cultured endothelial cells with the receptor-independent stimulus thimerosal (5 mumol/l, 40 min) evoked a long-lasting release of EDRF and small elevations of [Ca2+]i (twofold) after washout of the drug. Depolarization with K+ decreased thimerosal-induced EDRF release and [Ca2+]i in a reversible manner. In patch-clamped endothelial cells, bradykinin (1 nmol/l) induced transient hyperpolarizations that were significantly prolonged by BRL 34915 (1 mumol/l), an activator of K+ channels. BRL 34915 also elicited increases in [Ca2+]i, particularly in thimerosal-stimulated endothelial cells. These effects were abolished by K+. We conclude that the initial rise in [Ca2+]i in response to receptor-binding agonists, caused by mobilization of Ca2+ from intracellular stores, activates K+ channels, thereby inducing hyperpolarization.(ABSTRACT TRUNCATED AT 250 WORDS)
    [Abstract] [Full Text] [Related] [New Search]