A2-agonists

Central a2-Agonists Methyl dopa Clonidine (Catapres) Guanabenz Guanfacine (Tenex) Guanadrel No recommendations at this time Transient sedation initially First-line in pregnancy (methyldopa)... 

Drug therapy of an acute attack typically consists of an osmotic agent and secretory inhibitor (e.g., /1-blocker, a2 agonist, latanoprost, or CAI), with or without pilocarpine. 

The inhibitory effect of a2 agonists on noradrenaline release involves a hyperpolarization of the presynaptic membranes by opening potassium ion channels. The reduction in the release of noradrenaline following the administration of an a2 agonist is ultimately due to a reduction in the concentration of free cytosolic calcium, which is an essential component of the mechanism whereby the synaptic vesicles containing noradrenaline fuse to the s)maptic membrane before their release. 

A clinically useful action of a2-agonists is their ability to reduce the requirements for other anaesthetic agents during anaesthesia. In control mice, non-sedative doses of dexmedetomidine reduced the concentrations of the volatile anaesthetic, halothane, to induce anaesthesia by 30% (Lakhlani et al. 1997). This anaesthetic-sparing effect of a2-agonists was completely abolished in a2A-D79N mice. 

There are few absolute contraindications, but several points should be considered. Medications that produce changes in sinus node or AV nodal conduction may potentiate the cardiovascular adverse effects of the a2 agonists. This may be particularly relevant for concomitant administration of beta-blockers, which, similar to the agonists, have been used to treat aggression. 

Central Clonidine a2-agonist causes decreased sympathetic outflow. 

Dexmedetomidine is an a2 agonist with sedative and analgesic effects. It has a half-life of 2-3 hours and is... 

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