Serotonin is vasodilator or vasoconstrictor

\( \newcommand\) • • • • • • Adrenergic receptors are molecules that bind catecholamines. Their activation leads to overall stimulatory and sympathomimetic responses. Key Points • Adrenergic receptors consist of two main groups, α and β, multiple subgroups (α1, α2, β1, β2, β3), and several subtypes of the α2 subgroup (α2A, α2B, α2C). • Epinephrine binds both α and β adrenergic receptors to cause vasoconstriction and vasodilation. • When activated, the α1 receptor triggers smooth muscle contraction in blood vessels in the skin, gastrointestinal tract, kidney, and brain, among other areas. • When activated, the α2 receptor triggers inhibition of insulin and the induction of glucagon release in the pancreas, contraction of GI tract sphincters, and increased thrombocyte aggregation. • When activated, the α2 receptor triggers inhibition of insulin and induction of glucagon release in the pancreas, contraction of GI tract sphincters, and increased thrombocyte aggregation. Key Terms • adrenoreceptor: These are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine (noradrenaline) and epinephrine (adrenaline). Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system. • G protein-coupled receptors: These comprise a large protein family of transmembrane receptors that sense molecules outside the cell and activate inside signal transduction pathways ...

UNDER THE INFLUENCE of alcohol, the brain experiences impairments in the regions shown: Frontal Lobe (A) Loss of reason, caution, inhibitions, sociability, talkativeness and intelligence Parietal Lobe (B) Loss of fine motor skills, slower reaction time, shaking Temporal Lobe (C) Slurred speech, impaired hearing Occipital Lobe (D) Blurred vision, poor distance judgement Cerebellum (E) Lack of muscle coordination and balance Brain Stem (F) Loss of vital functions The product of the oldest chemical reaction studied by man<, alcohol, continues to challenge researchers. Since the original work on alcohol's neurological effects in the early 20th century, new theories have regularly emerged. What we have learned is that alcohol is a sedative-hypnotic in the acute intoxication phase for most patients. But it diminishes the quality of sleep. Individuals with sleep apnea often experience longer and more severe apneic episodes and hypoxia, or oxygen deprivation, after drinking alcohol. In other individuals, though, alcohol may act as a stimulant. Indeed, its association with violent and self-abusive behavior is well documented. At intoxicating levels, alcohol is a vasodilator (it causes blood vessels to relax and widen), but at even higher levels, it becomes a vasoconstrictor, shrinking the vessels and increasing blood pressure, exacerbating such conditions as migraine headaches and frostbite. Researchers have also thoroughly documented the effects of alcohol on the developing fetus....

Theories about migraine pain Older theories about migraines suggested that symptoms were possibly due to fluctuations in blood flow to the brain. Now many headache researchers realize that changes in blood flow and blood vessels don't initiate the pain, but may contribute to it. Current thinking regarding migraine pain has moved more toward the source of the problem, as improved technology and research have paved the way for a better understanding. Today, it is widely understood that chemical compounds and hormones, such as serotonin and estrogen, often play a role in pain sensitivity for migraine sufferers. One aspect of migraine pain theory explains that migraine pain happens due to waves of activity by groups of excitable brain cells. These trigger chemicals, such as serotonin, to narrow blood vessels. Serotonin is a chemical necessary for communication between nerve cells. It can cause narrowing of blood vessels throughout the body. When serotonin or estrogen levels change, the result for some is a migraine. Serotonin levels may affect both sexes, while fluctuating estrogen levels affect women only. For women, estrogen levels naturally vary over the life cycle, with increases during fertile years and decreases afterwards. Women of childbearing age also experience monthly changes in estrogen levels. Migraines in women are often associated with these fluctuating hormone levels and may explain why women are more likely to have migraines than men. Some research suggests th...

Serotonin and norepinephrine reuptake inhibitors (SNRIs) are a class of medications that are effective in treating depression. SNRIs are also sometimes used to treat other conditions, such as anxiety disorders and long-term (chronic) pain, especially nerve pain. SNRIs may be helpful if you have chronic pain in addition to depression. SNRIs ease depression by affecting chemical messengers (neurotransmitters) used to communicate between brain cells. Like most antidepressants, SNRIs work by ultimately effecting changes in brain chemistry and communication in brain nerve cell circuitry known to regulate mood, to help relieve depression. The Food and Drug Administration (FDA) has approved these SNRIs to treat depression: • Desvenlafaxine (Pristiq) • Duloxetine (Cymbalta) — also approved to treat anxiety and certain types of chronic pain • Levomilnacipran (Fetzima) • Venlafaxine (Effexor XR) — also approved to treat certain anxiety disorders and panic disorder All SNRIs work in a similar way and generally can cause similar side effects, though some people may not experience any side effects. Side effects are usually mild and go away after the first few weeks of treatment. Taking your medication with food may reduce nausea. If you can't tolerate one SNRI, you may be able to tolerate a different one, as each SNRI varies in chemical makeup. The most common possible side effects of SNRIs include: • Nausea • Dry mouth • Dizziness • Headache • Excessive sweating Other possible side ef...

Serotonin (as well as histamine, PAF, and bradykinin) does different things based on whether the endothelium is intact. So yes, if the endothelium is damaged, it causes vasoconstriction to reduce bleeding. If the endothelium ISN'T damaged, you don't need to worry about reducing bleeding. Instead, you need to increase blood flow so that white blood cells can extravasate and get to the injury. You get vasodilation when intact endothelium in the arterioles is exposed to histamine, serotonin, bradykinin and/or PAF (released due to injury). Then endothelium releases nitric oxide (NO), causing smooth muscle dilation. Also, PGI2 is a secondary effector of vasodilation: if the endothelium is intact, it can produce PGI2, which causes histamine, serotonin, bradykinin and/or PAF (the primary effectors) to cause arteriolar vasodilation. That makes sense if you want to increase blood flow and get more WBCs to the injured tissue.