Mechanism of Action

A number of theories have been put forward to account for the hypotensive action of a-methyldopa. Current evidence suggests that for a-methyldopa to be an anti-hypertensive agent, it must be converted to a-methyl-norepinephrine; however, its site of action appears to be in the brain rather than in the periphery. Systemically administered a-methyldopa rapidly enters the brain, where it accumulates in noradrenergic nerves, is converted to a-methylnorepinephrine, and is released. Released a-methylnorepinephrine activates CNS a-adrenoceptors whose function is to decrease sympathetic outflow. Why a-methylnorepinephrine decreases sympathetic outflow more effectively than does the naturally occurring transmitter is not entirely clear.

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