Q10.
10) Which of the drug is not
cardioselective beta1 blocker?
Answers
Answer:
The cardio-selective beta-blockers include atenolol, betaxolol, bisoprolol, esmolol, acebutolol, metoprolol, and nebivolol. FDA approved uses of beta-1-selective blockers include hypertension, chronic stable angina, heart failure, post-myocardial infarction, and decreased left ventricular function after a recent myocardial infarction. Non-FDA approved uses include migraine prophylaxis, treatment of arrhythmias, tremor reduction, and the symptomatic treatment of anxiety disorders . Their use is associated with decreased morbidity and mortality for post-myocardial infarction. Treatment with beta-1 blockers decreases the risk of stroke, coronary artery disease, and congestive heart failure (for example, metoprolol succinate has proven mortality benefit in the treatment of heart failure and it is the extended-release formulation of metoprolol).
The mortality benefits for metoprolol succinate in heart failure patients are attributed to their ability to block the toxic effects of chronic adrenergic stimulation of the heart. Initiation of metoprolol succinate in a heart failure patient is followed by clinical improvement, improved ejection fraction, and increased exercise tolerance. The benefits of left ventricular function improvement may take 2 to 3 months to observe after initiation of medication.
Slow calcium channel blockers and beta-blockers are medications that affect AV nodal function. The PR interval on the EKG defines the time needed for an impulse to travel through the atrium and AV nodal system to the ventricles. AV node conduction is the slowest and PR interval variations reflect changes in AV nodal activation time. Beta-blockers have a negative dromotropic effect on the AV node by prolonging the AV nodal refractory periods which could prolong the PR interval. The prolonged PR interval rarely results in more than first degree AV block in patients receiving maintenance therapy. In a few patients, combining calcium channel blocker and a beta-blocker may cause a second-degree AV block.
Mechanism of Action
Beta-1 receptors primarily are found in cardiac nodal tissue, cardiac myocytes, other heart conduction pathway tissues, and in the kidneys. Beta-1 blockers exert their effect by binding to the beta-1 receptor sites selectively and inhibiting the action of epinephrine and norepinephrine on these sites. Beta-1 receptors are G-protein-coupled receptors (specifically Gs alpha subunit) whose action is exerted through the cyclic AMP (cAMP) and cAMP-dependent protein kinase action with resultant calcium ion concentration increases [5] [6]. Increased intracellular calcium increase inotropy in the heart through calcium-induced exchange facilitated by the sarcoplasmic reticulum. Myosin light chains phosphorylated by PKA leads to contractility in muscle cells .
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