Vasodilation
Vasodilation is the widening of blood vessels as a result of the relaxation of the blood vessel's muscular walls. Vasodilation is a mechanism to enhance blood flow to areas of the body that are lacking oxygen and/or nutrients.
Vasodilation occurs naturally in your body in response to triggers such as low oxygen levels, a decrease in available nutrients, and increases in temperature. It causes the widening of your blood vessels, which in turn increases blood flow and lowers blood pressure. When blood pressure goes down, heart rate increases.
Arterioles have a lot of smooth muscles, smooth muscle tone controls blood flow to any tissue. An injured site needs more blood to bring in more antibodies and complement. Chemical mediators will act on vascular smooth muscle. Sometimes after injury there’s transient vasoconstriction (a few seconds) due to a neurogenic mechanism followed by significant, prolonged, vasodilation.
Vasodilation in response to increased flow is the function of the normal endothelium through the secretion of Nitric Oxide - Endothelium Derived Relaxing Factor (NO), prostacyclin (PGI2) and endothelial-derived hyperpolarizing factor (EDHF) to promote the relaxation of vascular smooth muscle cells. Reduction in these mechanisms contributes to aspects of endothelial dysfunction in several diseases, including hypertension, atherosclerosis and diabetes. Excessive vasodilation or insufficient constriction of the resistance blood vessels (mostly arterioles), causes hypotension.
The blood pressure lowering effect of hawthorn has been linked to nitric oxide-mediated vasodilation.
Vasodilation is mostly beneficial, as it helps deliver oxygen and nutrients throughout your body. But, vasodilation can be harmful in some cases, leading to severe hypotension (low blood pressure). Be on the lookout for signs of shock, including altered mental state, clammy skin and shallow or rapid breathing. Vasodilation causes headache, migraine and tinnitus.
Sleep typically involves a shift of dominance in the autonomic nervous system toward the parasympathetic nerves, with vasodilation.
Orbeli-Ginetsinsky phenomenon In the presence of humoral vasodilating agents, for example in the presence of inflammatory mediators produced locally, smooth muscle cells of arteriole become resistant to central neural vasoconstrictive influences. It was a very important discovery. It means that local humoral vasodilation can prevail over central neural vasoconstrictor signals. That's why, in hardwork, when in overall circulation sympathetic tone is dominating and activity of the sympathetic nervous system is prevailing, in non-working areas of the organism we have vasoconstriction, but in working muscles we still have vasodilation in spite of central sympathetic vasoconstrictor signals.
Nasal congestion after drinking alcoholic beverages due to the pharmacologic ability of ethanol to contribute to nasal vasodilation.
Mast cell stabilizers help regulate vasodilation. Mast cells are recruited during acute inflammation because histamine causes vasodilation and increased vascular permeability.
Chemoreceptors are responsible for signaling vasodilation and vasoconstriction.
GABA tends to raise body temperature by controlling vasodilation.
Bradykinin induces vasodilation. Angiotensin inhibitors increase bradykinin and can cause cough, angioedema and vasodilation. ACE Inhibitors / Angiotensin-converting enzyme inhibitors increase bradykinin.
Anandamide has also been found to activate TRPV1 on sensory neuron terminals, and subsequently cause vasodilation.