Vasoconstriction: A novel activity for low density lipoprotein

Sachinidis, Agapios; Locher, Rudolf; Mengden, Thomas; Steiner, Albert; Vetter, W

doi:10.1016/0006-291x(89)92137-2

Cited by 19 publications

(9 citation statements)

References 16 publications

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“…extrusion of cytosolic Ca'-" towards outside the cell or towards the intracellular stores) seem to be preserved since after the sustained [Ca""]i rise, the level of [Ca2*]i slowly decreased in several hours (by a as yet unknown mechanism). The intracellular acidification could be the consequence of the sustained [Ca'-+]~ rise which leads to H" metabolic generation as previously demonstrated in T cells [38]. Morphological changes shown by electron scanning microscopy of BAEC cultured in the presence of oxidized LDL are consistent with the observed [Ca2"]~ rise which is known to induce cell contraction [39,40] and regulation of endothelial barrier permeability [41].…”

Section: Febs Letters March 1992supporting

confidence: 76%

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

et al. 1992

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Bovine aortic endothelial c~lls (BAEC) pulsed for 5 h with mildly oxidized low density lipoproteins (LDL), exhibit~ a broad, sustained and high peak of [Ca:*]l occurring several hours after the end of the pulse and reachilll~ very high [Ca"+]t values (around 2500--3000 nmol/I) and a concomitant drop of eytosolic pH (around 0.2-0.3 pH units) without any loss of cell viability. When BAEC were continuously pulsed with oxidized LDL, the peak of [Ca2*]~ was more sustained than in short pulse experiments and was associated with irreversible morphological ~hanges usually associat~l with cytotoxi¢ events (blebbin$) and with a marked loss of viability. The potential involvement of thes, biochemical and morphological changes in atherogenesis are discussed.

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Section: Febs Letters March 1992supporting

confidence: 76%

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

et al. 1992

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“…Attenuation of endothelium-dependent dilations results in an increase in vascular smooth muscle tone, but enhanced smooth muscle tone can also be caused by enhanced responses to constrictor agonists. On the other hand, they further increase Ca 2ϩ in smooth muscle cells (10,11). Enhanced vascular smooth muscle contractility has been observed in hypercholesterolemic monkeys (5), dogs (6), miniature swine (7), and rabbits (1,8).…”

mentioning

confidence: 99%

Oxidized LDL and its Compound Lysophosphatidylcholine Potentiate AngII-Induced Vasoconstriction by Stimulation of RhoA

Galle¹,

Mameghani²,

Bolz³

et al. 2003

Journal of the American Society of Nephrology

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RhoA stimulates vascular tone by increasing smooth muscle Ca(2+) sensitivity, e.g., in atherosclerosis. This study was an investigation of the influence of oxidized LDL (OxLDL), which accumulates in atherosclerotic plaques, on vascular tone induced by angiotensin II (AngII), with particular emphasis on the RhoA pathway. OxLDL had no influence on unstimulated vascular tone of isolated rabbit aorta, but it potentiated contractile responses induced by AngII. The Ca(2+)-antagonist felodipin partially prevented potentiation of contractile responses, whereas the AT(1) receptor antagonist losartan blunted AngII responses in presence and in absence of OxLDL. Rho-kinase inhibition by Y27632 abolished potentiation of contractile responses, and RhoA inhibition by C3-like transferase partially prevented it, suggesting that OxLDL activated RhoA. Activation of RhoA was further analyzed by detection of its translocation to the cell membrane after stimulation with OxLDL. Western blot analysis of aorta homogenates, as well as direct visualization in cultured smooth muscle cells using confocal laser scan microscopy, revealed that OxLDL potently activated RhoA. The effect of OxLDL was mimicked by its compound lysophosphatidylcholine, and C3 inhibited both lysophosphatidylcholine and OxLDL-induced RhoA stimulation. In conclusion, OxLDL stimulates the RhoA pathway, resulting in potentiation of AngII-induced vasoconstriction. Lysophosphatidylcholine mimics the OxLDL effect, consistent with a causal role of this OxLDL compound. Stimulation of RhoA by OxLDL may contribute to vasospasm in atherosclerotic arteries.

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“…This was compared with that of N-LDL, which in previous studies from our laboratory had been shown to activate VSMCs and to elevate [Ca 2+ ]|. 15 - 17 The determination of this parameter might further elucidate the role of LDL and the mechanisms of action of its oxidized forms in cardiovascular disease.…”

Section: Oxidation Of Low Density Lipoprotein Enhances Its Potential mentioning

confidence: 99%

Oxidation of low density lipoprotein enhances its potential to increase intracellular free calcium concentration in vascular smooth muscle cells.

Weisser

Locher

Mengden

et al. 1992

Arterioscler Thromb

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Vasoconstriction: A novel activity for low density lipoprotein

Cited by 19 publications

References 16 publications

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

A delayed and sustained rise of cytosolic calcium is elicited by oxidized LDL in cultured bovine aortic endothelial cells

Oxidized LDL and its Compound Lysophosphatidylcholine Potentiate AngII-Induced Vasoconstriction by Stimulation of RhoA

Oxidation of low density lipoprotein enhances its potential to increase intracellular free calcium concentration in vascular smooth muscle cells.

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