<P> The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: </P> <Ul> <Li> α 1 (\ displaystyle \ alpha _ (1)) receptors . Under NE binding α 1 (\ displaystyle \ alpha _ (1)) receptors cause vasoconstriction (i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). α 1 (\ displaystyle \ alpha _ (1)) receptors are activated in response to shock or low blood pressure as a defensive reaction trying to restore the normal blood pressure . Antagonists of α 1 (\ displaystyle \ alpha _ (1)) receptors (doxazosin, prazosin) cause vasodilation (i.e. decrease in vascular smooth muscle tone with increase of vessel diameter and decrease of the blood pressure). (See also receptor antagonist) </Li> <Li> α 2 (\ displaystyle \ alpha _ (2)) receptors . Agonists of α 2 (\ displaystyle \ alpha _ (2)) receptors in the vascular smooth muscle lead to vasoconstriction . However, in clinical practice drugs applied intravenously that are agonists of α 2 (\ displaystyle \ alpha _ (2)) receptors (clonidine) lead to powerful vasodilation, which causes a decrease in blood pressure by presynaptic activation of α 2 (\ displaystyle \ alpha _ (2)) receptors in the sympathetic ganglia . This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the α 2 (\ displaystyle \ alpha _ (2)) receptors in the vascular smooth muscle . </Li> <Li> β 2 (\ displaystyle \ beta _ (2)) receptors . Agonism of β 2 (\ displaystyle \ beta _ (2)) receptors causes vasodilation and low blood pressure (i.e. the effect is opposite of the one resulting from activation of α 1 (\ displaystyle \ alpha _ (1)) and α 2 (\ displaystyle \ alpha _ (2)) receptors in the vascular smooth muscle cells). Usage of β 2 (\ displaystyle \ beta _ (2)) receptor agonists as hypotensive agents is less widespread due to adverse effects such as unnecessary bronchodilation in lungs and increase in blood sugar levels . </Li> </Ul> <Li> α 1 (\ displaystyle \ alpha _ (1)) receptors . Under NE binding α 1 (\ displaystyle \ alpha _ (1)) receptors cause vasoconstriction (i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). α 1 (\ displaystyle \ alpha _ (1)) receptors are activated in response to shock or low blood pressure as a defensive reaction trying to restore the normal blood pressure . Antagonists of α 1 (\ displaystyle \ alpha _ (1)) receptors (doxazosin, prazosin) cause vasodilation (i.e. decrease in vascular smooth muscle tone with increase of vessel diameter and decrease of the blood pressure). (See also receptor antagonist) </Li> <Li> α 2 (\ displaystyle \ alpha _ (2)) receptors . Agonists of α 2 (\ displaystyle \ alpha _ (2)) receptors in the vascular smooth muscle lead to vasoconstriction . However, in clinical practice drugs applied intravenously that are agonists of α 2 (\ displaystyle \ alpha _ (2)) receptors (clonidine) lead to powerful vasodilation, which causes a decrease in blood pressure by presynaptic activation of α 2 (\ displaystyle \ alpha _ (2)) receptors in the sympathetic ganglia . This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the α 2 (\ displaystyle \ alpha _ (2)) receptors in the vascular smooth muscle . </Li>

Contraction of the smooth muscles in the tunica media of blood vessels causes
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