Description
Increased bronchoconstriction can therefore result from beta-blocker medications like atenolol that inhibit this activity. Atenolol is a beta-blocker that selectively binds to the 1-adrenergic receptor as an antagonist, up to a reported 26 fold more than 2 receptors. This is why it is known as a cardioselective beta-blocker. Both of these occurrences result in a contraction reduction, which when combined with the initial contraction increase, permits faster cycling and, as a result, a higher heart rate with increased contractility. PKA is thought to mediate the activation of L-type calcium channels and ryanodine receptors in cardiomyocytes through the phosphorylation of these proteins. Troponin I is additionally phophorylated to lessen the protein's affinity for calcium. L-type calcium channels are also a major contributor to cardiac depolarization and their activation can increase frequency of action potentials and possibly the incidence of ectopic potentials. The ryanodine receptors are then triggered to release calcium that has been stored in the sarcoplasmic reticulum (SR), leading to an initial increase in intracellular calcium and increased contractility. This is accomplished by L-type calcium channels. The inositol trisphosphate receptor and phospholipase C are phosphorylated by PKA, which prevents the release of intracellular calcium and inhibits the excitatory Gq coupled pathway. By phosphorylating phospholamban, which in turn increases the SR Ca2+ ATPase's affinity to increase calcium reuptake into the SR, PKA also contributes to the cessation of contraction. Due to the higher population of this receptor in cardiac tissue, cardioselectivity is produced by selective activity at the 1 receptor. The phosphorylation of myosin light-chain kinase, which lowers its affinity for calcium, is one of the similar inhibitory events that mediate relaxation in the bronchial smooth muscle. Some binding to β2 and possibly β3 receptors can still occur at therapeutic dosages but the effects mediated by antagonizing these are significantly reduced from those of non-selective agents. β1 and β2 receptors are Gs coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA).
Dosage
-Doses above 100 mg once daily did not produce any appreciable additional antihypertensive effects. -Treatment with beta blockers post MI should generally continue for 1 to 3 years if there are no contraindications. 50 mg orally twice a day or 100 mg orally once a day Comments: -Oral therapy should continue for at least 7 days after myocardial infarction (MI) if IV beta blockers are contraindicated or inappropriate. Detailed Atenolol dosage information Initial dose: 50 mg once daily; increase to 100 mg once daily after one week if desired results are not seen; maintenance dose: 50 to 200 mg once daily; maximum dose: 200 mg daily; comments: -Some patients may need 200 mg daily to achieve desired results. Initial dose: 50 mg orally once daily Maintenance dose: 50 to 100 mg orally once daily Maximum dose: 100 mg per day Comments: -Increase to 100 mg if desired response is not seen after 1 to 2 weeks. Initial dose: Consider reducing the starting dose to 25 mg orally once a day Application: For the long-term treatment of angina pectoris brought on by coronary atherosclerosis. Use: To lower cardiovascular mortality, manage patients with definite or suspected acute myocardial infarction who are hemodynamically stable. Use: To treat hypertension either on its own or in conjunction with other antihypertensive medications. Atenolol dosage for angina pectoris prevention in adults: Atenolol dosage for angina pectoris in adults: Atenolol dosage for hypertension in adults: For Myocardial Infarction, the typical adult dosage of atenolol is: Atenolol dosage for hypertension in the elderly:
Missed dose
Do not take two doses at one time. If it is almost time for your next dose, skip the missed dose and take the medication as soon as you can.
Overdose
Call local emergency services at 911 if the victim has collapsed or is not breathing. In case of overdose, call your local poison control center at 1-800-222-1222. Lack of energy, difficulty breathing, wheezing, slow heartbeat, fainting, swelling of the hands, feet, ankles, or lower legs, shakiness, dizziness, rapid heartbeat, sweating or confusion, blurred vision, headache, excessive tiredness, pale skin, and sudden hunger are all possible signs of overdosing.
Storage
This medication should not, however, be flushed down the toilet. Instead, the best way to dispose of your medication is through a medicine take-back program. All medications should be kept out of the sight and reach of children, as many of the containers (such as weekly pill containers and those for eye drops, creams, patches, and inhalers) are not child-resistant and are simple for small children to open. Keep this medication in the container it came in, tightly closed, and out of reach of children. If you do not have access to a take-back program, visit the FDA's Safe Disposal of Medicines website at http://goo.gl/c4Rm4p for more information. Store it at room temperature, away from sources of extreme heat, and dry (not in the bathroom). To find out about take-back programs in your area, speak with your pharmacist or the garbage/recycling department in your city. Always lock safety caps and store medications up and away, out of sight, and away from young children to prevent poisoning. http://www.upandaway.org Unused medications should be disposed of in special ways to prevent pets, children, and other people from consuming them.
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(C) Effect of 0.5 mA/heptanol on in situ luminescence induced by 10 ^A/atenolol. (B) Effect of 0.25 mA/octanol on KCI-induced flash activity of dissociated photocytes. t t sw Atenolol t t t t sw Atenolol sw Atenolol I mm Figure I. Photometric recordings of the effect of gap junction uncouplers on stimulated biolumines- cence of Rcnillu koellikeri- (A) Effect of 0.25 mA/octanol on in .tilu KCI-induced flash activity.
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