Dobutamine is predominantly a β 1 -adrenergic agonist , with weak β 2 activity, and α 1 selective activity, although it is used clinically in cases of cardiogenic shock for its β 1 inotropic effect in increasing heart contractility and cardiac output. Dobutamine is administered as a racemic mixture consisting of both (+) and (−) isomers ; the (+) isomer is a potent β 1 agonist and α 1 antagonist, while the (−) isomer is an α 1 agonist. [4] The administration of the racemate results in the overall β 1 agonism responsible for its activity. (+)-Dobutamine also has mild β 2 agonist activity, which makes it useful as a vasodilator. [5]

Milrinone is a phosphodiesterase-3 inhibitor. This drug inhibits the action of phosphodiesterase-3 and thus prevents degradation of cAMP. With increased cAMP levels there is an increase in the activation of PKA. This PKA will phosphorylate many components of the cardiomyocyte such as calcium channels and components of the myofilaments . Phosphorylation of calcium channels permits an increase in calcium influx into the cell. This increase in calcium influx results in increased contractility. PKA also phosphorylates potassium channels promoting their action. Potassium channels are responsible for repolarization of the cardiomyocytes therefore increasing the rate at which cells can depolarize and generate contraction. PKA also phosphorylates components on myofilaments allowing actin and myosin to interact more easily and thus increasing contractility and the inotropic state of the heart. Milrinone allows stimulation of cardiac function independently of β-adrenergic receptors which appear to be down-regulated in those with heart failure.