Catecholamines bind to cardiac beta-adrenoceptor to introduce positive inotropic, chronotropic, dromotropic and lucinotropic effects of the heart. Therapeutic catecholamines causes less effects to failing myocardium in comparison to normal myocardium. Down-regulation of cardiac beta-adrenoceptor (decrease in receptor number) and uncoupling of beta-adrenoceptor to G protein (increase in Gi alpha) have been demonstrated in failing human myocardium. Rapid improvement can be obtained in cardiac function by intravenous catecholamines, usually with dopamine and/or dobutamine in patients with acute heart failure. But, tachyphylaxis occurs in 72 hours which limits usefulness of the drugs. Dopamine has DA1-receptor activity which increases renal blood flow and natriuresis. Dobutamine is superior to dopamine in positive lucinotropic effects in reducing PCWP in patients with heart failure. Mechanisms of beta blocker therapy with special reference to molecular mechanisms are discussed.