<unk> s, more specifically the auto receptors of<unk>  2 neurons, are used in the treatment of glaucoma by decreasing the production of aqueous fluid by the ciliary bodies of the eye and also by increasing uveoscleral outflow. Medications such as clonidine and dexmedetomidine target pre-synaptic auto receptors, therefore leading to an overall decrease in norepinephrine which clinically can cause effects such as sedation, analgesia, lowering of blood pressure and bradycardia. There is also low quality evidence that they can reduce shivering post operatively The reduction of the stress response caused by<unk>  2 agonists were theorised to be beneficial peri operatively by reducing cardiac complications, however this has shown not to be clinically effective as there was no reduction in cardiac events or mortality but there was an increased incidence of hypotension and bradycardia
Alpha-adrenergic agonist
Beta-adrenergic agonist
Beta2-adrenergic agonist
Dopamine agonist
Muscarinic antagonist
Norepinephrine–dopamine disinhibitor
Adrenergic release inhibitor
Dopamine antagonist