Editing Haemodynamic response (section)

===Smooth muscle===

Dilation occurs when [[nitric oxide]] (NO) is released from endothelial cells and diffuses into nearby vascular smooth muscle. Several proposed pathways of NO-induced vasodilation have been proposed through haemodynamic investigation. It has been shown that NO inhibits 20-HETE synthesis, which may interfere with astrocytes' constriction pathways and lead to vasodilation. It has also been proposed that NO may amplify astrocyte Ca{{sup|2+}} influx and activate Ca{{sup|2+}}-dependent [[potassium channels]], releasing K{{sup|+}} into the interstitial space and inducing [[hyperpolarization (biology)|hyperpolarization]] of smooth muscle cells.<ref name="jap.physiology" /> In addition to this, it has already been shown that NO stimulates increased [[cyclic GMP]] (cGMP) levels in the smooth muscle cells, inducing a signaling cascade that results in the activation of [[cGMP-dependent protein kinase]] (PKG) and an ultimate decrease in smooth muscle Ca{{sup|2+}} concentration.<ref>{{cite journal |author1=Grange Robert W. |author2=Isotani Eiji | year = 2000 | title = Nitric Oxide Contributes to Vascular Smooth Muscle Relaxation in Contracting Fast-twitch Muscles | journal = Physiological Genomics | volume = 5 | issue = 1| pages = 35–44 |doi=10.1152/physiolgenomics.2001.5.1.35 |pmid=11161004 |s2cid=7117482 }}</ref> This leads to a decrease in muscle contraction and a subsequent dilation of the blood vessel. Whether the vessels are constricted or dilated dictates the amount of oxygen and glucose that is able to reach the neuronal tissue.