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There is a consensus that ANG II may trigger vascular inflammation by inducing oxidative stress and upregulation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-κB).
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A key mechanism by which particles could trigger vascular dysfunction is by down-regulating NO synthase.
This came as no surprise, as apnea may trigger a decrease in systemic vascular resistance upon severe acute stimulation of receptors [78].
Nociceptive stimuli may trigger headache, and neural and vascular changes are thought to be important in the pathophysiology of headache.
Thus, advanced glycation end products and hemodynamic abnormalities related to type 1 diabetes may trigger signaling pathways involved in the appearance of vascular calcification (27).
However, ox-LDL uptake by LOX-1 also mediates EC apoptosis, potentially via nuclear factor (NF)- κB activation [ 101, 152] and resulting in direct vascular denudation and injury that may trigger or enhance the inflammatory and oxidative stress reactions.
This intra-abdominal pressure alteration may trigger an unclear neural reflex resulting in a cerebral vascular change.
CSD biochemical changes may trigger the activations of meningeal trigeminal endings and trigemino-vascular system, causing the headache phase.
Precipitating factors, such as sexual activity, may induce vascular changes with profound hemodynamic fluctuations, which may trigger the pain if an arterial narrowing is present.
It is suggested that TRPV4-mediated [Ca2+]i rise in endothelial cells may trigger both NO- and/or EDHF-dependent vasodilatation that seems to be vascular bed-dependent.
While numerous studies have suggested that TRPV4 in vascular smooth muscle couples with hyperpolarising K + channels to induce vasodilatation (Earley et al., 2005; Earley et al., 2009), activation of TRPV4 simultaneously across multiple cells (as opposed to very localised activation) may trigger Ca 2+-dependent vasoconstriction to maintain a basal level of vascular tone.
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