Serotonin blood vessel dilation

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

Besides NE and DA agonistic effects, the psychomimetics are also believed to impinge upon the serotonergic neurons. Serotonin stimulation can promote sleep as well as increase blood pressure and heart rate, produce tremors, constrict blood vessels, and cause pupil dilation just as... 

Methysergide (Sansert ) is believed to alter the ability of serotonin to cause inflammation, platelet aggregation (blood clotting), and dilation of blood vessels. However, methysergide has some undesirable side effects, such as motor incoordination and dizziness and can cause heart problems. Usually, the drug is intentionally discontinued for 4-6 weeks twice a year because of these problems. Thus, methysergide is used only in special cases. 

Similar events occur in the carotid cells. The only difference is that they release catecholamines instead of serotonin, causing dilatation of the blood vessels. 

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