Bisoprolol is beneficial in treatment for high blood pressure (hypertension), reduced blood flow to the heart (cardiac ischemia); congestive heart failure, and preventive treatment before and primary treatment after heart attacks, decreasing the chances of recurrence. Bisoprolol targets hypertension (elevated blood pressure). In cardiac ischemia, the drug is used to reduce the activity of the heart muscle, so reduces oxygen and nutrient demand, and reduced blood supply can still transport sufficient amounts of oxygen and nutrients.
Overdose of bisoprolol leads to fatigue, hypotension, low blood sugar,bronchospasms, and bradycardia. Bronchospasms and low blood sugar because at high doses drug can be an antagonist for β2 adrenergic receptors located in lung and in liver. Bronchospasm is due to blockage in lungs of β2 receptor and low blood sugar because of decreased stimulation of glycogenolysis and gluconeogenesis in the liver via β2 receptor.
Beta-blockers should generally be avoided in people with a history of asthma or bronchospasm as they may make the disease worse. A beta 1 selective beta blocker like bisoprolol may be tried in those in whom other options are not available.
Mechanism of action
Bisoprolol is cardioprotective because it selectively and competitively blocks catecholamine (adrenaline) stimulation of β1 adrenergic receptors (adrenoreceptors), which are mainly found in the heart muscle cells and heart conduction tissue (cardiospecific), but also found in juxtaglomerular cells in the kidney. Normally, adrenaline and noradrenaline stimulation of the β1 adrenoreceptor activates a signalling cascade (Gs protein and cAMP) which ultimately leads to increased contractility and increased heart rate of the heart muscle and heart pacemaker, respectively. Bisoprolol competitively blocks the activation of this cascade, so decreases the adrenergic tone/stimulation of the heart muscle and pacemaker cells. Decreased adrenergic tone shows less contractility of heart muscle and lowered heart rate of pacemakers.
Selectivity of various β-blockers
Bisoprolol β1-selectivity is especially important in comparison to other nonselective beta blockers. The effects of the drug are limited to areas containing β1 adrenoreceptors, which is mainly the heart and part of the kidney. Bisoprolol minimizes the side effects that might occur from administration of a nonspecific beta blocker where blockage of the other adrenoreceptors (β2, β3, α1, α2) occurs. The other receptors elicit a variety of responses in the body, and their blockage could cause a wide range of reactions, but β1 adrenoreceptors are cardiospecific for the most part, making bisoprolol ideal for treatment of cardiac events.
Bisoprolol inhibits renin secretion by about 65% and tachycardia by about 30%.
Bisoprolol has both lipid- and water-soluble properties. It has an approximate half-life of 10–12 hours, and when ingested has high bioavailability (approx. 90%). When being eliminated, the body evenly distributes it (50–50) between kidney excretion and liver biotransformation (then excreted).
Society and culture
Bisoprolol is available as a generic medication.
Bisoprolol was patented in 1976 and approved for medical use in 1986. It was approved for medical use in the United States in 1992.
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