![]() ![]() Īlpha-1 receptor agonists taken at toxic doses lead to increased sympathetic tone, which results in tachycardia, early hypertension progressing to hypotension, mydriasis, anxiety, and increased glycogenolysis. Both clonidine and guanfacine are used for behavior modification in children with attention deficit disorder, as well as in adults with PTSD as well. Peripheral presynaptic alpha-2 receptors may also reduce sympathetic tone. Alpha-2 agonists, including clonidine and guanfacine - are used as anti-hypertensives, as well. Alpha-2 stimulation reduces the sympathetic outflow from the vasomotor center centrally and increases vagal tone. Alpha-blockers are also used off-label for the treatment of post-traumatic stress disorder (PTSD). Īlpha-blockers have significant use in the setting of pre-operative pheochromocytoma care. ![]() Alpha-antagonists, colloquially known as alpha-blockers, work in the peripheral vasculature and inhibit the uptake of catecholamines in smooth muscle cells resulting in vasodilation and blood pressure lowering. Alpha-antagonists, including doxazosin, prazosin, and phentolamine - are primarily used in the treatment of hypertension and urinary retention. Alpha-1 agonists, such as phenylephrine, are also used to treat upper airway congestion as stimulating the receptor leads to a decreased mucus secretion. ![]() It is worth noting that these compounds are not purely selective for the alpha receptor, and often engage beta-adrenergic receptors as well. The use of alpha-1 agonists is common in all types of shock, cardiopulmonary resuscitation, and heart failure decompensation. In instances in which there is hypoperfusion secondary to decreased cardiac output or decreased systemic vasculature resistance, alpha-1 receptors become stimulated. Alpha-1 receptors bind catecholamines including, both epinephrine and norepinephrine. The indication for the use of an alpha-adrenergic receptor modifying medication depends on which receptor is the target: the alpha-1 receptor or the alpha-2 receptor. ![]()
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