Adrenergic receptors are the receptors that constitute sympathetic system. Most agonists of these receptors can be called sympathomimetics. Isoprenaline, dobutamine and dopexamine are synthetic catecholamines. Catecholamines cause their clinical effects through interaction with α, β, and dopaminergic receptors. Cardiac Glycosides are the drugs derived from plants (digitalis purpurea/lanata). The main feature of glycosides is to increase the heart contractility (inotropy) without much increase in oxygen consumption by the heart. Digoxin is most commonly used glycoside. Clinical effects, uses, and adverse effects of cardiac glycosides are briefly described. Phosphodiesterase (PDE) is a family of enzymes which inactivate cyclic adenosine monophosphate (cAMP). Phosphodiesterase inhibitors (PDIs) increase the level of cAMP by inhibiting its breakdown within the cell. This increases calcium levels leading to increase in inotropy, chronotropy and lusitropy. In vascular smooth muscle, increase in cGMP levels causes vasodilation so there is pulmonary, systemic vasodilation. Another drug discussed in the chapter is calcium sensitizer (levosimendan) that increases contractility without increasing cAMP levels appreciably at clinically recommended doses. Arginine vasopressin is a nonapeptide, synthesized as a pro-hormone in the paraventricular and supraoptic nuclei of the posterior hypothalamus. Dopexamine is a synthetic catecholamine structurally related to dopamine. Acting as β2 agonist, this drug causes arterial vasodilation, increased renal perfusion by selective renal vasodilation. It is used mainly for acute heart failure and in patient undergoing cardiac surgery.