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Microvasc Res. 2000 Jan;59(1):38-44.

Nitric oxide causes a cGMP-independent intracellular calcium rise in porcine endothelial cells-a paradox?

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Institut fuer Pharmakologie, Universitaet zu Koeln, Koeln, 50931, Germany.


This study was undertaken to investigate the influence of exogenous NO on intracellular calcium levels of porcine aortic endothelial cell culture monolayers. Spontaneous NO liberating substances with different half-life periods (NOC-9 [10 micromol/L] approximately 1 min, SNAP [10 micromol/L] approximately 4 h), and an aqueous NO gas solution [130 nmol/L] were added onto the monolayers. All three solutions induced a rapid and similar calcium rise in the endothelial cells. NOC-9 as a rapidly NO releasing compound was selected to be investigated more thoroughly. The NOC-9 calcium rise is not dependent on the activation of the guanylate cyclase since preincubation with a specific guanylate cyclase inhibitor [ODQ, 10 micromol/L] did not alter the effect and a cGMP analogue [8-bromo-cGMP 10 micromol/L] did not significantly elevate calcium levels. The NOC-9 induced calcium rise could be completely blocked by removal of extracellular calcium and partly blocked by SKF 96365 [10 micromol/L], an unspecific inhibitor of the receptor operated calcium channels. Incubation with N-nitroarginine [100 micromol/L] slightly but significantly reduced basal calcium levels in the cell cultures. Therefore, we conclude that exogenous NO elevates [Ca(2+)](i) in cultured porcine aortic endothelial cells. This effect is not dependent on cGMP, and a calcium influx is involved. Moreover, constitutively formed endogenous NO seems to be necessary to maintain basal calcium levels.

[Indexed for MEDLINE]

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