VPA-treated group (B&D; magnified from B, note: some vasodilatations
However, it produces vasodilatation
in blood vessels in connection with its muscle relaxant effect (Guzel and McKinstry, 2017; Guzel et al., 2018).
Dural mast cells induce meningeal vasodilatation
via not only release of histamine from mast cells but also axon reflex resulted in release of CGRP and SP from activated C-fibers in the dura mater.
It may subsequently lead to imbalance in vasoconstriction and vasodilatation
which are associated with an increased risk of cardiovascular disorders.1,2
The endothelium-dependent vasodilatation
was evaluated by relaxation of aortic rings in response to acetylcholine. Aorta was excised immediately in deep isoflurane anesthesia and placed at 4[degrees]C into Kreb's-Henseleit buffer (NaCl 118 mmol/L, KCl 4.7 mmol/L, CaCl[sub]2 2.5 mmol/L, MgCl[sub]2 1.2 mmol/L, KH[sub]2 PO[sub]4 1.2 mmol/L, NaHCO[sub]3 25 mmol/L, glucose 11 mmol/L, and pH 7.4) and saturated with a mixture of gas including 95% O[sub]2 and 5% CO[sub]2 in advance.
It causes vasodilatation
in many vessels as well as in the portal vein.
The observation that pathological vasodilatation
of the pulmonary bed may be attenuated without improved oxygenation however suggests a more complex pathophysiology, and recently, impaired hypoxic pulmonary vasoconstriction has been implicated .
Some researchers  consider that NO mediates vasodilatation
by increasing soluble guanylate cyclase (sGC) in the smooth muscle of vessels.
Endothelial dysfunction results in an imbalance between vasoconstriction and vasodilatation
, causing tissue reperfusion, cytotoxic oedema, and brain injury.5,7 Results of several investigations regarding the role of NO as biochemical marker to assess brain injury in newborns are controversial.14,15
BACKGROUND: We explored whether chronic hyperglycemia is associated with defects in endothelium-dependent vasodilatation
in vivo and whether defects in the hemodynamic effects of insulin explain insulin resistance.
Since the main pathophysiology of HRS is splanchnic arterial vasodilatation
and renal arterial vasoconstriction that causes increase in resistive index (RI) of renal arterial system and the terlipressin (intravenously administered vasopressin 1 receptor agonist) causes selective vasoconstriction of splanchnic arterial vessels, which tends to reverse alterations in renal haemodynamic.
Although physical inactivity increases oxidative stress and endothelial dysfunction,  intense physical training decreases circulating antioxidants and endothelium-dependent vasodilatation
;  therefore, it is necessary to optimize exercise training in FMS patients.