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.

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.

Pirbuterol (trade name Maxair) is a short-acting β2 adrenoreceptor agonist with bronchodilating action used in the treatment of asthma. The pharmacologic effects of beta-adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Pirbuterol is used in asthma for reversal of acute bronchospasm, and also as a maintenance medication to prevent future attacks. It should be used in patients 12 years of age and older with or without concurrent theophylline and/or inhaled corticosteroid. After inhalation of doses up to 800 μg (twice the maximum recommended dose) systemic blood levels of pirbuterol are below the limit of assay sensitivity (2–5 ng/ml). A mean of 51% of the dose is recovered in urine as pirbuterol plus its sulfate conjugate following administration by aerosol. Pirbuterol is not metabolized by catechol-O-methyltransferase.

Pirbuterol (trade name Maxair) is a short-acting β2 adrenoreceptor agonist with bronchodilating action used in the treatment of asthma. The pharmacologic effects of beta-adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Pirbuterol is used in asthma for reversal of acute bronchospasm, and also as a maintenance medication to prevent future attacks. It should be used in patients 12 years of age and older with or without concurrent theophylline and/or inhaled corticosteroid. After inhalation of doses up to 800 μg (twice the maximum recommended dose) systemic blood levels of pirbuterol are below the limit of assay sensitivity (2–5 ng/ml). A mean of 51% of the dose is recovered in urine as pirbuterol plus its sulfate conjugate following administration by aerosol. Pirbuterol is not metabolized by catechol-O-methyltransferase.

Pirbuterol (trade name Maxair) is a short-acting β2 adrenoreceptor agonist with bronchodilating action used in the treatment of asthma. The pharmacologic effects of beta-adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Pirbuterol is used in asthma for reversal of acute bronchospasm, and also as a maintenance medication to prevent future attacks. It should be used in patients 12 years of age and older with or without concurrent theophylline and/or inhaled corticosteroid. After inhalation of doses up to 800 μg (twice the maximum recommended dose) systemic blood levels of pirbuterol are below the limit of assay sensitivity (2–5 ng/ml). A mean of 51% of the dose is recovered in urine as pirbuterol plus its sulfate conjugate following administration by aerosol. Pirbuterol is not metabolized by catechol-O-methyltransferase.

Bitolterol is a beta 2-adrenergic agonist. Since it in itself is biologically inactive, bitolterol is considered a pro-drug. When administered it is activated within the lung by esterase hydrolysis to the active compound colterol catecholamine N-t-butyl-arterenol. Bitolterol was marked under the name tornalate and was indicated to prevent and treat of reversible bronchospasm associated with asthma or chronic obstructive pulmonary diseases. But that drug was withdrawn from the market by Elan Pharmaceuticals in 2001.

Dipivefrin is a prodrug with little or no pharmacologically activity until it is hydrolyzed into epinephrine inside the human eye. The liberated epinephrine, an adrenergic agonist, appears to exert its action by stimulating α -and/or β2-adrenergic receptors, leading to a decrease in aqueous production and an enhancement of outflow facility. The dipivefrin prodrug delivery system is a more efficient way of delivering the therapeutic effects of epinephrine, with fewer side effects than are associated with conventional epinephrine therapy. Dipivefrin is used as initial therapy for the control of intraocular pressure in chronic open-angle glaucoma.

Ritodrine (trade name Yutopar) is beta-2 adrenergic agonist used to stop premature labor. Ritodrine binds to beta-2 adrenergic receptors on the outer membrane of the myometrial cell, activates adenyl cyclase to increase the level of cAMP which decreases intracellular calcium and leads to a decrease of uterine contractions. In addition to stimulating the beta-2–adrenergic receptors of the uterine smooth muscle, ritodrine stimulates beta-adrenergic receptors of bronchial and vascular smooth muscles. The cardiostimulatory effects, including increased cardiac output, increased maternal and fetal heart rates, and widening of the maternal pulse pressure, are probably due to relaxation of the vascular smooth muscle. Relaxation of vascular smooth muscle stimulates the beta-1–adrenergic receptors and the reflex response to blood pressure. Also, during intravenous administration, ritodrine transiently increases maternal and fetal blood glucose and maternal plasma insulin concentrations. Other metabolic changes include increased cAMP, lactic acid, and free fatty acids, and decreased serum potassium concentration. Most side effects of β2 agonists result from their concurrent β1 activity and include the increase in heart rate, rise in systolic pressure, decrease in diastolic pressure, chest pain secondary to myocardial infarction, and arrhythmia. Beta-agonists may also cause fluid retention secondary to decrease in water clearance, which when added to the tachycardia and increased myocardial work, may result in heart failure. In addition, they increase gluconeogenesis in the liver and muscle resulting in hyperglycemia, which increases insulin requirements in diabetic patients. The passage of β agonists through the placenta does occur and may be responsible for fetal tachycardia, as well as hypoglycemia or hyperglycemia at birth.

Isoetharine is a beta-2 adrenergic receptor agonist, which was developed by Max Bockmuhl, Gustav Erhart and Leonhard Stein at the Hochst laboratories of I.G. Farbenindustrie in 1934. By binding to beta-2 adrenergic receptors on bronchial cell membranes, isoetharine increases the level of cAMP and thus stimulates the relaxation of smooth-muscle cells, stabilizes mast cells and inhibits histamine release. Isoetharine was approved by FDA for the symptomatic relief of bronchiospasms in patients with chronic bronchitis or emphysema (aerosol and solution for inhalation), however, later on the drug was discontinued.

Isoetharine is a beta-2 adrenergic receptor agonist, which was developed by Max Bockmuhl, Gustav Erhart and Leonhard Stein at the Hochst laboratories of I.G. Farbenindustrie in 1934. By binding to beta-2 adrenergic receptors on bronchial cell membranes, isoetharine increases the level of cAMP and thus stimulates the relaxation of smooth-muscle cells, stabilizes mast cells and inhibits histamine release. Isoetharine was approved by FDA for the symptomatic relief of bronchiospasms in patients with chronic bronchitis or emphysema (aerosol and solution for inhalation), however, later on the drug was discontinued.