Atenolol is a Beta-1 cardio-selective adreno-receptor blocking agent discovered and developed by ICI in 1976. Atenolol was launched in the market under the trade name Tenormin in 1976, and became the best-selling Beta-blocker in the world in the 1980s and 1990s. TENORMIN is indicated for the treatment of hypertension, to lower blood pressure; also for the long-term management of patients with angina pectoris and also is indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Like metoprolol, atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles. Hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.

Nadolol is a nonselective beta-adrenergic receptor antagonist with a long half-life, and is structurally similar to propranolol. Clinical pharmacology studies have demonstrated beta-blocking activity by showing (1) reduction in heart rate and cardiac output at rest and on exercise, (2) reduction of systolic and diastolic blood pressure at rest and on exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. Nadolol has no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, nadolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. Like other beta-adrenergic antagonists, nadolol competes with adrenergic neurotransmitters such as catecholamines for binding at sympathetic receptor sites. Like propranolol and timolol, nadolol binds at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting the effects of the catecholamines epinephrine and norepinephrine and decreasing heart rate, cardiac output, and systolic and diastolic blood pressure. It also blocks beta-2 adrenergic receptors located in bronchiole smooth muscle, causing vasoconstriction. By binding beta-2 receptors in the juxtaglomerular apparatus, nadolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production. Nadolol therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively. Nadolol is used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension.

Mrtoprolol is a beta-adrenergic receptor blocking agent. In vitro and in vivo animal studies have shown that it has a preferential effect on beta-1 adrenoreceptors, chiefly located in cardiac muscle. Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. Mrtoprolol is indicated for the treatment of hypertension, angina pectoris and myocardial infarction

Propranolol is a nonselective, beta-adrenergic receptor-blocking agent possessing no other autonomic nervous system activity. At dosages greater than required for beta blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. Among the factors that may be involved in contributing to the antihypertensive action include: (1) decreased cardiac output, (2) inhibition of renin release by the kidneys, and (3) diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain. Although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol. Effects of propranolol on plasma volume appear to be minor and somewhat variable. In angina pectoris, propranolol generally reduces the oxygen requirement of the heart at any given level of effort by blocking the catecholamine-induced increases in the heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. Propranolol may increase oxygen requirements by increasing left ventricular fiber length, end diastolic pressure, and systolic ejection period. The net physiologic effect of beta-adrenergic blockade is usually advantageous and is manifested during exercise by delayed onset of pain and increased work capacity. Propranolol exerts its antiarrhythmic effects in concentrations associated with beta-adrenergic blockade, and this appears to be its principal antiarrhythmic mechanism of action. In dosages greater than required for beta blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain. The mechanism of the anti-migraine effect of propranolol has not been established. Propranolol is indicated in the management of hypertension. It may be used alone or used in combination with other antihypertensive agents, particularly a thiazide diuretic. Also is indicated to decrease angina frequency and increase exercise tolerance in patients with angina pectoris; for the prophylaxis of common migraine headache. In addition, is used to improve NYHA functional class in symptomatic patients with hypertrophic subaortic stenosis. Due to the high penetration across the blood–brain barrier, propranolol causes sleep disturbances such as insomnia and vivid dreams, and nightmares. Dreaming (rapid eye movement sleep, REM) was reduced and increased awakening.

Penbutolol is a new beta-adrenergic blocking drug approved for the treatment of hypertension. It is a noncardioselective beta-blocker and has intrinsic sympathomimetic activity. Penbutolol is marketed under the trade names Levatol, Levatolol, Lobeta, Paginol, Hostabloc, Betapressin. Penbutolol acts on the β1 adrenergic receptors in both the heart and the kidney. When β1 receptors are activated by catecholamines, they stimulate a coupled G protein that leads to the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). The increase in cAMP leads to activation of protein kinase A (PKA), which alters the movement of calcium ions in heart muscle and increases the heart rate. Penbutolol blocks the catecholamine activation of β1 adrenergic receptors and decreases heart rate, which lowers blood pressure. Levatol (Penbutolol) is indicated in the treatment of mild to moderate arterial hypertension. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.

Oxprenolol is clinically a well-established beta blocker that shares with other members of this group the ability to control a variety of disorders, in particular, hypertension and angina. Pharmacologically it is a nonselective beta blocker that possesses partial agonist activity (intrinsic sympathomimetic activity). Pharmacokinetically, oxprenolol behaves as a moderately lipophilic agent. Oxprenolol undergoes first pass metabolism with only 30% of an oral dose reaching the systemic circulation. The drug is approximately 80% protein bound and is eliminated primarily by glucuronidation in the liver. Less than 4% of oxprenolol is excreted unchanged in the urine. Oxprenolol may reduce the heart rate and prolong the effective and functional atrioventricular nodal refractory period. Oxprenolol has less negative inotropic and chronotropic effects than propranolol. Plasma renin activity is reduced; however, changes in plasma aldosterone level are not significant. Long term metabolic effects require further study. Chest pain (angina), high blood pressure (hypertension), irregular heart beats and anxiety are indications for Oxprenolol usage. To date Oxprenolol is discontinued by FDA.

Alprenolol is a beta adrenoreceptor blocking agent and 5HT1A antagonist, developed by AstraZeneca and now available as generic drug. It is used for treatment of hypertension, angina pectoris due to coronary atherosclerosis and acute myocardial infarction.

Cloranolol is a specific beta-adrenergic antagonist. It is used as an antiarrhythmic agent. Its antiarrhythmic effectiveness stronger than propranol and equal or surpass the effectivity of pindolol. It has a negligible cardiodepressant activity as compared to other beta-adrenergic antagonists. Cloranolol has mainly cardiorespiratory side effects judging from the beta-blocker characteristics

Mepindolol is a selective beta1-adrenoreceptor blocker with intrinsic sympathetic activity. Treatment with mepindolol dose not significantly affect the lipid levels - the total cholesterol in plasma was decreased by mepindolol but HDL-cholesterol increased. During beta-receptor blockade with mepindolol-sulfate angina was compensated, the unfavourable hemodynamic effects seen during placebo did not occur. No signs of congestive heart failure were found during mepindolol-sulfate-therapy. Mepindolol-sulfate showed a pronounced blood-pressure lowering effect.

Celiprolol is beta blocker, used to treat high blood pressure. Celiprolol is a selective β1 receptor antagonist, β2 receptor partial agonist. Celiprolol is not approved by the FDA, but is available worldwide under brand names Cardem, Selectol, Celipres, Celipro, Celol, Cordiax, Dilanorm. It is used to treat mild to moderate hypertension and angina prectoris. In 2010 celiprolol has demonstrated positive results in the prevention of vascular complications of Ehlers-Danlos syndrome. Celiprolol has fewer CNS-related side effects than other beta blockers presumably because of limited penetration through blood-brain barrier because of its solubility.