The present invention provides a strategy to compensate for deficiency in the alpha-2C receptor by administering an agonist of different receptors; the alpha-2A and/or dopamine d2 receptors. These receptors are fully functional and receptive to stimulation by an agonist. Agonism of the alpha-2A and/or dopamine d2 receptors by clonidine, Nolomirole or other suitable agonist may down regulate epinephrine production, and hence compensate for the deficiency in the alpha-2C receptor. Such methods are useful for treating a variety of cardiovascular disorders.