Atenolol

Last updated

Atenolol
Atenolol.svg
Atenolol 3d structure.png
Clinical data
Trade names Tenormin, others
AHFS/Drugs.com Monograph
MedlinePlus a684031
License data
Pregnancy
category
  • AU:C
Routes of
administration 		Oral, intravenous
Drug class Selective β1 receptor antagonist
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • US: WARNING [1]
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 40–50%
Protein binding 6–16% [2]
Metabolism Minimal [2]
Onset of action IV Tooltip Intravenous injection: <5 minutes [2]
Oral: <1 hour [2]
Elimination half-life 6–7 hours [2]
Duration of action >24 hours [2]
Excretion Urine (>85% IV, 50% oral) [2]
Identifiers
  • (RS)-2-{4-[2-Hydroxy-3-(propan-2-ylamino)propoxy]phenyl}acetamide
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.044.941 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C14H22N2O3
Molar mass 266.341 g·mol−1
3D model (JSmol)
Chirality Racemic mixture
  • O=C(N)Cc1ccc(cc1)OCC(O)CNC(C)C
  • InChI=1S/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) Yes check.svgY
  • Key:METKIMKYRPQLGS-UHFFFAOYSA-N Yes check.svgY
   (verify)

Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain. [3] Although used to treat high blood pressure, it does not seem to improve mortality in those with the condition. [4] [5] Other uses include the prevention of migraines and treatment of certain irregular heart beats. [3] [6] It is taken orally (by mouth) or by intravenous injection (injection into a vein). [3] [6] It can also be used with other blood pressure medications. [6]

Contents

Common side effects include feeling tired, heart failure, dizziness, depression, and shortness of breath. [3] Other serious side effects include bronchial spasm. [3] Use is not recommended during pregnancy [3] and alternative drugs are preferred when breastfeeding. [7] It works by blocking β1-adrenergic receptors in the heart, thus decreasing the heart rate and workload. [3]

Atenolol was patented in 1969 and approved for medical use in 1975. [8] It is on the World Health Organization's List of Essential Medicines. [9] It is available as a generic medication. [3] In 2021, it was the 47th most commonly prescribed medication in the United States, with more than 14 million prescriptions. [10] [11]

Medical uses

Atenolol is used for a number of conditions including hyperthyroidism, [12] hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, and the symptoms of alcohol withdrawal. [13]

The role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than other agents such as ACE inhibitors, calcium channel blockers, thiazide diuretics and angiotensin receptor blockers, particularly in the elderly. [14] [15] [16]

Available forms

Atenolol is available in the form of 25, 50, and 100 mg oral tablets. [17] [2] It is also available in the form of oral tablets containing a combination of 50 or 100 mg atenolol and 50 mg chlortalidone. [17] Atenolol was previously available in a 0.5 mg/mL solution for injection as well, but this formulation was discontinued. [17]

Side effects

Hypertension treated with a β-blocker such as atenolol, alone or in conjunction with a thiazide diuretic, is associated with a higher incidence of new onset type 2 diabetes mellitus compared to those treated with an ACE inhibitor or angiotensin receptor blocker. [18] [19]

β-blockers, of which atenolol is mainly studied, provides weaker protection against stroke and mortality in patients over 60 years old compared to other antihypertensive medications. [20] [21] [22] [14] Diuretics may be associated with better cardiovascular and cerebrovascular outcomes than β-blockers in the elderly. [23]

Overdose

Symptoms of overdose are due to excessive pharmacodynamic actions on β1 and also β2-receptors. These include bradycardia (slow heartbeat), severe hypotension with shock, acute heart failure, hypoglycemia and bronchospastic reactions. Treatment is largely symptomatic. Hospitalization and intensive monitoring is indicated. Activated charcoal is useful to absorb the drug. Atropine will counteract bradycardia, glucagon helps with hypoglycemia, dobutamine can be given against hypotension and the inhalation of a β2-mimetic such as hexoprenalin or salbutamol will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims. [24] [25]

Interactions

Interactions with atenolol include catecholamine-depleting drugs like reserpine, calcium channel blockers, disopyramide, amiodarone, clonidine, prostaglandin synthase inhibitors like indomethacin, and digitalis glycosides. [26] Most of these interactions involve either additive cardiovascular effects or reduction of atenolol's effects. [26]

Atenolol is mainly eliminated renally without being metabolized by the liver or by cytochrome P450 enzymes. [26] [27] [28] As a result, it has little or no potential for cytochrome P450-related drug interactions, for instance with inhibitors and inducers of these enzymes. [27] [28]

Beta blockers like atenolol can reduce or block the cardiovascular effects of sympathomimetics and amphetamines, such as hypertension and tachycardia. [29] [30] [31] [32] [33] [34] [35]

Atenolol has been found to be safe in combination with the non-selective monoamine oxidase inhibitor (MAOI) phenelzine and actually improved orthostatic hypotension and hypertensive reactions with phenelzine. [36] [37] [38] However, more research is still needed to assess whether addition of a beta blocker like atenolol to MAOI therapy is safe and effective for improving orthostatic hypotension with MAOIs. [36] [38]

Pharmacology

Pharmacodynamics

Atenolol is a beta blocker, that is, an antagonist of the β-adrenergic receptors. [39] [2] It is specifically a selective antagonist of the β1-adrenergic receptor with no intrinsic sympathomimetic activity (i.e., partial agonist activity) or membrane-stabilizing activity. [39] [2] However, the preferential action of atenolol is not absolute, and at high doses it can also block β2-adrenergic receptors. [2]

Beta-blocking effects of atenolol include reduction in resting and exercise heart rate and cardiac output, reduction of systolic and diastolic blood pressure at rest and with exercise, inhibition tachycardia induced by isoproterenol (a non-selective β-adrenergic receptor agonist), and reduction of reflex orthostatic tachycardia. [2] The beta-blocking effects of atenolol, as measured by reduction of exercise-related tachycardia, are apparent within 1 hour and are maximal within 2 to 4 hours following a single oral dose. [2] The pharmacodynamic effects of atenolol, including beta-blocking and antihypertensive effects, last for at least 24 hours following oral doses of 50 or 100 mg. [2] With intravenous administration, maximal reduction in exercise-related tachycardia occurs within 5 minutes and following a single 10 mg dose has dissipated within 12 hours. [2] The duration of action of atenolol is dose-related and is correlated with circulating levels of atenolol. [2]

Pharmacokinetics

The absorption of atenolol with oral administration is rapid and consistent but is incomplete. [2] About 50% of an oral dose of atenolol is absorbed from the intestines, with the rest excreted in feces. [2] Maximal concentrations of atenolol occur 2 to 4 hours following an oral dose, whereas peak concentrations occur within 5 minutes with intravenous administration. [2] The pharmacokinetic profile of atenolol results in it having relatively consistent plasma drug levels with about 4-fold variation between individuals. [2]

The plasma protein binding of atenolol is 6 to 16%. [2] Atenolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier and entering the brain. [39] This in turn may result in fewer effects in the central nervous system as well as a lower risk of neuropsychiatric side effects. [39]

Atenolol undergoes little to no metabolism by the liver. [2] This is in contrast to other beta blockers like propranolol and metoprolol, but is similar to nadolol. [2] Instead of hepatic metabolism, atenolol is eliminated mainly via renal excretion. [2] Atenolol is excreted 50% in urine with oral administration and more than 85% in urine with intravenous administration. [2]

The elimination half-life of atenolol is about 6 to 7 hours. [2] The half-life of atenolol does not change with continuous administration. [2] With intravenous administration, atenolol levels rapidly decline (5- to 10-fold) during the first 7 hours and thereafter decline at a rate similar to that with oral administration. [2] The elimination of atenolol is slowed in renal impairment, with the elimination rate being closely related to the glomerular filtration rate and with significant accumulation occurring when the creatinine clearance rate is under 35 mL/min/1.73 m2. [2]

Chemistry

The experimental log P of atenolol is 0.16 and its predicted log P ranges from −0.03 to 0.57. [40] [41] [42]

Society and culture

Atenolol has been given as an example of how slow healthcare providers are to change their prescribing practices in the face of medical evidence that indicates that a drug is not as effective as others in treating some conditions. [43] In 2012, 33.8 million prescriptions were written to American patients for this drug. [43] In 2014, it was in the top (most common) 1% of drugs prescribed to Medicare patients. [43] Although the number of prescriptions has been declining steadily since limited evidence articles contesting its efficacy was published, it has been estimated that it would take 20 years for doctors to stop prescribing it for hypertension. [43] Despite its diminished efficacy when compared to newer antihypertensive drugs, atenolol and other beta blockers are still a relevant clinical choice for treating some conditions, since beta blockers are a diverse group of medicines with different properties that still requires further research. [14] As consequence, reasons for the popularity of beta blockers cannot be fully attributed to a slow healthcare system – patient compliance factor, such as treatment cost and duration, also affect adherence and popularity of therapy. [44]

Related Research Articles

<span class="mw-page-title-main">ACE inhibitor</span> Class of medications used primarily to treat high blood pressure

Angiotensin-converting-enzyme inhibitors are a class of medication used primarily for the treatment of high blood pressure and heart failure. This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.

<span class="mw-page-title-main">Beta blocker</span> Medications for abnormal heart rhythms

Beta blockers, also spelled β-blockers, are a class of medications that are predominantly used to manage abnormal heart rhythms (arrhythmia), and to protect the heart from a second heart attack after a first heart attack. They are also widely used to treat high blood pressure, although they are no longer the first choice for initial treatment of most patients.

Antihypertensives are a class of drugs that are used to treat hypertension. Antihypertensive therapy seeks to prevent the complications of high blood pressure, such as stroke, heart failure, kidney failure and myocardial infarction. Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34% and of ischaemic heart disease by 21%, and can reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease. There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used medications are thiazide diuretics, calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists (ARBs), and beta blockers.

<span class="mw-page-title-main">Metoprolol</span> Medication of the selective β1 receptor blocker type

Metoprolol, sold under the brand name Lopressor among others, is a medication used to treat high blood pressure, angina, and a number of conditions involving an abnormally fast heart rate. It is also used to prevent further heart problems after myocardial infarction and to prevent headaches in those with migraines. It is a selective β1 receptor blocker medication. It is taken by mouth or is given intravenously.

<span class="mw-page-title-main">Sotalol</span> Medication

Sotalol, sold under the brand name Betapace among others, is a medication used to treat and prevent abnormal heart rhythms. Evidence does not support a decreased risk of death with long term use. It is taken by mouth or given by injection into a vein.

<span class="mw-page-title-main">Nadolol</span> Non-selective beta blocker used in the treatment of high blood pressure and chest pain

Nadolol, sold under the brand name Corgard among others, is a medication used to treat high blood pressure, heart pain, atrial fibrillation, and some inherited arrhythmic syndromes. It has also been used to prevent migraine headaches and complications of cirrhosis. It is taken orally.

<span class="mw-page-title-main">Phenylephrine</span> Decongestant medication

Phenylephrine, sold under the brand names Neosynephrine and Sudafed PE among numerous others, is a medication used as a decongestant for uncomplicated nasal congestion, used to dilate the pupil, used to increase blood pressure, and used to relieve hemorrhoids. It can be taken by mouth, as a nasal spray, given by injection into a vein or muscle, applied to the skin, or as a rectal suppository.

<span class="mw-page-title-main">Isoprenaline</span> Medication for slow heart rate

Isoprenaline, also known as isoproterenol and sold under the brand name Isuprel among others, is a sympathomimetic medication which is used in the treatment of acute bradycardia, heart block, and rarely for asthma, among other indications. It is used by injection into a vein, muscle, fat, or the heart, by inhalation, and in the past under the tongue or into the rectum.

Alpha-1 blockers constitute a variety of drugs that block the effect of catecholamines on alpha-1-adrenergic receptors. They are mainly used to treat benign prostatic hyperplasia (BPH), hypertension and post-traumatic stress disorder. Alpha-1 adrenergic receptors are present in vascular smooth muscle, the central nervous system, and other tissues. When alpha blockers bind to these receptors in vascular smooth muscle, they cause vasodilation.

<span class="mw-page-title-main">Phentolamine</span> An α-adrenergic antagonist medication

Phentolamine, sold under the brand name Regitine among others, is a reversible nonselective α-adrenergic antagonist.

<span class="mw-page-title-main">Bisoprolol</span> Beta-1 selective adrenenergic blocker medication used to treat cardiovascular diseases

Bisoprolol, sold under the brand name Zebeta among others, is a beta blocker which is selective for the beta-1 receptor and used for cardiovascular diseases, including tachyarrhythmias, high blood pressure, angina, and heart failure. It is taken by mouth.

<span class="mw-page-title-main">Carvedilol</span> Blood pressure medication

Carvedilol, sold under the brand name Coreg among others, is a beta blocker medication, that may be prescribed for the treatment of high blood pressure (hypertension) and chronic heart failure with reduced ejection fraction. Beta-blockers as a collective medication class are not recommended as routine first-line treatment of high blood pressure for all patients, due to evidence demonstrating less effective cardiovascular protection and a less favourable safety profile when compared to other classes of blood pressure-lowering medications.

<span class="mw-page-title-main">Nebivolol</span> Chemical compound

Nebivolol is a beta blocker used to treat high blood pressure and heart failure. As with other β-blockers, it is generally a less preferred treatment for high blood pressure. It may be used by itself or with other blood pressure medication. It is taken by mouth.

<span class="mw-page-title-main">Adrenergic antagonist</span> Type of drug

An adrenergic antagonist is a drug that inhibits the function of adrenergic receptors. There are five adrenergic receptors, which are divided into two groups. The first group of receptors are the beta (β) adrenergic receptors. There are β1, β2, and β3 receptors. The second group contains the alpha (α) adrenoreceptors. There are only α1 and α2 receptors. Adrenergic receptors are located near the heart, kidneys, lungs, and gastrointestinal tract. There are also α-adreno receptors that are located on vascular smooth muscle.

<span class="mw-page-title-main">Alpha blocker</span> Class of pharmacological agents

Alpha-blockers, also known as α-blockers or α-adrenoreceptor antagonists, are a class of pharmacological agents that act as antagonists on α-adrenergic receptors (α-adrenoceptors).

<span class="mw-page-title-main">Landiolol</span> Chemical compound

Landiolol (INN) is an ultra short-acting, β1-superselective intravenous adrenergic antagonist, which decreases the heart rate effectively with less negative effect on blood pressure or myocardial contractility. In comparison to other beta blockers, landiolol has the shortest elimination half-life, ultra-rapid onset of effect, and predictable effectiveness with inactive metabolites. The pure S-enantiomer structure of landiolol is believed to develop less hypotensive side effects in comparison to other β-blockers. This has a positive impact on the treatment of patients when reduction of heart rate without decrease in arterial blood pressure is desired. It is used as landiolol hydrochloride.

<span class="mw-page-title-main">Discovery and development of beta-blockers</span>

β adrenergic receptor antagonists were initially developed in the 1960s, for the treatment of angina pectoris but are now also used for hypertension, congestive heart failure and certain arrhythmias. In the 1950s, dichloroisoproterenol (DCI) was discovered to be a β-antagonist that blocked the effects of sympathomimetic amines on bronchodilation, uterine relaxation and heart stimulation. Although DCI had no clinical utility, a change in the compound did provide a clinical candidate, pronethalol, which was introduced in 1962.

Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the sympathetic nervous system in the body. The sympathetic nervous system(SNS) is an autonomic nervous system that we cannot control by will. It triggers a series of responses after the body releases chemicals named noradrenaline and epinephrine. These chemicals will act on adrenergic receptors, with subtypes Alpha-1, Alpha-2, Beta-1, Beta-2, Beta-3, which ultimately allow the body to trigger a "fight-or-flight" response to handle external stress. These responses include vessel constriction in general vessels whereas there is vasodilation in vessels that supply skeletal muscles or in coronary vessels. Additionally, the heart rate and contractile force increase when SNS is activated, which may be harmful to cardiac function as it increases metabolic demand.

Adrenergic neurone blockers, commonly known as adrenergic antagonists, are a group of drugs that inhibit the sympathetic nervous system by blocking the activity of adrenergic neurones. They prevent the action or release of catecholamines such as norepinephrine and epinephrine. They are located throughout the body, causing various physiological reactions including bronchodilation, accelerated heartbeat, and vasoconstriction. They work by inhibiting the synthesis, release, or reuptake of the neurotransmitters or by antagonising the receptors on postsynaptic neurones. Their medical uses, mechanisms of action, adverse effects, and contraindications depend on the specific types of adrenergic blockers used, including alpha 1, alpha 2, beta 1, and beta 2.

Cardiovascular agents are drugs used to treat diseases associated with the heart or blood vessels. These medications are available for purchase only with a physician’s prescription. They include, but are not limited to, drugs that target hypertension (antihypertensives), hyperlipidemia (antihyperlipidemics) and blood clotting (blood-thinners) to reduce the risk of cardiovascular diseases.

References

  1. ↑ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA . Retrieved 22 October 2023.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 "DailyMed - TENORMIN- atenolol tablet". DailyMed. 30 June 2021. Archived from the original on 27 January 2022. Retrieved 20 November 2023.
  3. 1 2 3 4 5 6 7 8 "Atenolol Monograph for Professionals". Drugs.com. AHFS. Archived from the original on 18 April 2019. Retrieved 23 December 2018.
  4. ↑ Tomiyama H, Yamashina A (2014). "Beta-Blockers in the Management of Hypertension and/or Chronic Kidney Disease". International Journal of Hypertension. 2014: 919256. doi: 10.1155/2014/919256 . PMC   3941231 . PMID   24672712.
  5. ↑ DiNicolantonio JJ, Fares H, Niazi AK, Chatterjee S, D'Ascenzo F, Cerrato E, et al. (2015). "β-Blockers in hypertension, diabetes, heart failure and acute myocardial infarction: a review of the literature". Open Heart. 2 (1): e000230. doi:10.1136/openhrt-2014-000230. PMC   4371808 . PMID   25821584.
  6. 1 2 3 British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. pp. 151–153. ISBN   9780857113382.
  7. ↑ "Atenolol use while Breastfeeding". Drugs.com. Archived from the original on 23 December 2018. Retrieved 23 December 2018.
  8. ↑ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 461. ISBN   9783527607495.
  9. ↑ World Health Organization (2021). World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization. hdl: 10665/345533 . WHO/MHP/HPS/EML/2021.02.
  10. ↑ "The Top 300 of 2021". ClinCalc. Archived from the original on 15 January 2024. Retrieved 14 January 2024.
  11. ↑ "Atenolol – Drug Usage Statistics". ClinCalc. Retrieved 14 January 2024.
  12. ↑ Rehman B, Sanchez DP, Shah S (2021). "Atenolol". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30969666. Archived from the original on 10 October 2022. Retrieved 5 September 2021.
  13. ↑ "Atenolol". The American Society of Health-System Pharmacists. Archived from the original on 18 April 2019. Retrieved 8 May 2018.
  14. 1 2 3 Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH (January 2017). "Beta-blockers for hypertension". The Cochrane Database of Systematic Reviews. 1 (1): CD002003. doi:10.1002/14651858.CD002003.pub5. PMC   5369873 . PMID   28107561. Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people [...] Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3)
  15. ↑ Ladva S (28 June 2006). "NICE and BHS launch updated hypertension guideline". National Institute for Health and Clinical Excellence. Archived from the original on 11 May 2008. Retrieved 19 August 2012.
  16. ↑ Cruickshank JM (August 2007). "Are we misunderstanding beta-blockers". International Journal of Cardiology. 120 (1): 10–27. doi:10.1016/j.ijcard.2007.01.069. PMID   17433471.
  17. 1 2 3 "Drugs@FDA: FDA-Approved Drugs". accessdata.fda.gov. Retrieved 8 July 2024.
  18. ↑ Lindholm LH, Ibsen H, Borch-Johnsen K, Olsen MH, Wachtell K, Dahlöf B, et al. (September 2002). "Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study". Journal of Hypertension. 20 (9): 1879–86. doi:10.1097/00004872-200209000-00035. PMID   12195132. S2CID   23613019.
  19. ↑ Elliott WJ, Meyer PM (January 2007). "Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis". Lancet. 369 (9557): 201–7. doi:10.1016/s0140-6736(07)60108-1. PMID   17240286. S2CID   37044384.
  20. ↑ Lindholm LH, Carlberg B, Samuelsson O (October 2005). "Should β blockers remain first choice in the treatment of primary hypertension? A meta-analysis". The Lancet. 366 (9496): 1545–1553. doi:10.1016/S0140-6736(05)67573-3. PMID   16257341. S2CID   34364430.
  21. ↑ Khan N, McAlister FA (June 2006). "Re-examining the efficacy of beta-blockers for the treatment of hypertension: a meta-analysis". CMAJ. 174 (12): 1737–42. doi:10.1503/cmaj.060110. PMC   1471831 . PMID   16754904.
  22. ↑ Kuyper LM, Khan NA (May 2014). "Atenolol vs nonatenolol β-blockers for the treatment of hypertension: a meta-analysis". The Canadian Journal of Cardiology. 30 (5 Suppl): S47-53. doi: 10.1016/j.cjca.2014.01.006 . PMID   24750981.
  23. ↑ Messerli FH, Grossman E, Goldbourt U (June 1998). "Are beta-blockers efficacious as first-line therapy for hypertension in the elderly? A systematic review". JAMA. 279 (23): 1903–7. doi:10.1001/jama.279.23.1903. PMID   9634263.
  24. ↑ DeLima LG, Kharasch ED, Butler S (July 1995). "Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations". Anesthesiology. 83 (1): 204–7. doi:10.1097/00000542-199507000-00025. PMID   7605000.
  25. ↑ Baselt R (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, Calif.: Biomedical Publications. pp. 116–117.
  26. 1 2 3 "TENORMIN® (atenolol) Tablets Drug Label" (PDF). Food and Drug Administration. December 2023. Retrieved 8 July 2024.
  27. 1 2 Brodde OE, Kroemer HK (2003). "Drug-drug interactions of beta-adrenoceptor blockers". Arzneimittelforschung. 53 (12): 814–822. doi:10.1055/s-0031-1299835. PMID   14732961. Atenolol is only minimally, if at all, metabolized and renally excreted in mostly unchanged form; thus an interaction with drugs that interfere with the hepatic metabolism is not to be expected. It is also very unlikely that the genetic polymorphisms of the CYP-family might affect the pharmacokinetics of atenolol. In fact it has been shown that plasma concentrations of nonmetabolized atenolol was not significantly different between "extensive" and "poor debrisoquine metabolizers" – in contrast to the plasma concentrations of metoprolol that were significantly increased in "poor metabolizers" (Dayer et al. 1985, Lewis et al. 1985). Furthermore, in healthy volunteers cimetidine (CAS 70059- 30-2) did not affect plasma concentrations of atenolol but significantly increased plasma concentrations of metoprolol or propranolol (Kirch et al. 1981).
  28. 1 2 Scheen AJ (September 2011). "Cytochrome P450-mediated cardiovascular drug interactions". Expert Opin Drug Metab Toxicol. 7 (9): 1065–1082. doi:10.1517/17425255.2011.586337. PMID   21810031. β-Blockers still represent widely prescribed drugs as they cover a wide spectrum of CV indications. Obviously, it is not trivial which β-blocker to choose as they differ both with regard to their PD and PK profiles [82]. It is well known when comparing the characteristics of atenolol, bisoprolol, metoprolol (each β-1 selective) and carvedilol (β-1 and β-2 nonselective). Among these β-blockers, atenolol is mainly eliminated by renal excretion; bisoprolol is in part excreted as parent compound via the renal route (50%); the other 50% are hepatically metabolized; whereas metoprolol and carvedilol are metabolized by CYP2D6. DDIs are mainly observed with those β-blockers that are metabolized via CYP enzymes. However, it should be emphasized that, in general, β-blockers are well-tolerated safe drugs with a large therapeutic index [83].
  29. ↑ Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ (May 2015). "Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review". Drug Alcohol Depend. 150: 1–13. doi:10.1016/j.drugalcdep.2015.01.040. PMID   25724076.
  30. ↑ Vetter VL, Elia J, Erickson C, Berger S, Blum N, Uzark K, et al. (May 2008). "Cardiovascular monitoring of children and adolescents with heart disease receiving medications for attention deficit/hyperactivity disorder [corrected]: a scientific statement from the American Heart Association Council on Cardiovascular Disease in the Young Congenital Cardiac Defects Committee and the Council on Cardiovascular Nursing". Circulation. 117 (18): 2407–2423. doi:10.1161/CIRCULATIONAHA.107.189473. PMID   18427125. Amphetamines (Adderall, Dexedrine): Electrophysiological Effects of Amphetamines: Amphetamines have been associated with tachyarrhythmias and sudden death.113–115 Many of the electrophysiological effects of amphetamines may be initiated by the release of norepinephrine stores from presynaptic vesicles and blocking of norepinephrine reuptake.116,117 In addition, amphetamines are potent blockers of dopamine uptake and strong central nervous system stimulants. Dopaminergic Effects of Amphetamines: In addition to the β-agonist effects of amphetamines, the dopamine receptors D1 and D2 contribute to the cardiovascular effects of methamphetamine by producing a pressor response accounting for the increase in blood pressure. The D1 receptor also is involved in mediating the positive tachycardic effects of methamphetamine.117
  31. ↑ Schindler CW, Zheng JW, Tella SR, Goldberg SR (August 1992). "Pharmacological mechanisms in the cardiovascular effects of methamphetamine in conscious squirrel monkeys". Pharmacol Biochem Behav. 42 (4): 791–796. doi: 10.1016/0091-3057(92)90031-a . PMID   1325059.
  32. ↑ Mores N, Campia U, Navarra P, Cardillo C, Preziosi P (June 1999). "No cardiovascular effects of single-dose pseudoephedrine in patients with essential hypertension treated with beta-blockers". Eur J Clin Pharmacol. 55 (4): 251–254. doi:10.1007/s002280050624. PMID   10424315.
  33. ↑ Hassan NA, Gunaid AA, El-Khally FM, Al-Noami MY, Murray-Lyon IM (April 2005). "Khat chewing and arterial blood pressure. A randomized controlled clinical trial of alpha-1 and selective beta-1 adrenoceptor blockade". Saudi Med J. 26 (4): 537–541. PMID   15900355.
  34. ↑ O'Connell MB, Gross CR (1990). "The effect of single-dose phenylpropanolamine on blood pressure in patients with hypertension controlled by beta blockers". Pharmacotherapy. 10 (2): 85–91. PMID   2349137.
  35. ↑ O'Connell MB, Gross CR (1991). "The effect of multiple doses of phenylpropanolamine on the blood pressure of patients whose hypertension was controlled with beta blockers". Pharmacotherapy. 11 (5): 376–81. PMID   1684039.
  36. 1 2 Gadde KM, Krishnan KR (1998). "Management of Side Effects of Monoamine Oxidase Inhibitors". In Balon R (ed.). Practical Management of the Side Effects of Psychotropic Drugs. Medical Psychiatry Series. CRC Press. pp. 67–83 (71). ISBN   978-0-8247-4630-8 . Retrieved 8 July 2024. Interestingly, in one study, orthostatic hypotension was eliminated in a group of 61 patients treated for migraine headaches with phenelzine, when a beta-blocker, atenolol, was added (15). The authors have reported that hypertensive reactions were also less frequent when the two drugs were combined. We need further experience with this combination to determine whether addition of a beta-blocker is a safe and an effective strategy for alleviation of postural hypotension in depressed patients receiving an MAOI.
  37. ↑ O'Brien P, Oyebode F (2003). "Psychotropic medication and the heart". Advances in Psychiatric Treatment. 9 (6): 414–423. doi:10.1192/apt.9.6.414. ISSN   1355-5146. Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na+ or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (Merikangas & Merikangas, 1995).
  38. 1 2 Merikangas KR, Merikangas JR (November 1995). "Combination monoamine oxidase inhibitor and beta-blocker treatment of migraine, with anxiety and depression". Biol Psychiatry. 38 (9): 603–610. doi: 10.1016/0006-3223(95)00077-1 . PMID   8573662.
  39. 1 2 3 4 Cojocariu SA, Maștaleru A, Sascău RA, Stătescu C, Mitu F, Leon-Constantin MM (February 2021). "Neuropsychiatric Consequences of Lipophilic Beta-Blockers". Medicina (Kaunas). 57 (2): 155. doi: 10.3390/medicina57020155 . PMC   7914867 . PMID   33572109.
  40. ↑ "Atenolol". PubChem. Retrieved 1 August 2024.
  41. ↑ "Atenolol: Uses, Interactions, Mechanism of Action". DrugBank Online. 13 August 2004. Retrieved 1 August 2024.
  42. ↑ "DL-Atenolol". ChemSpider. 21 July 2022. Retrieved 1 August 2024.
  43. 1 2 3 4 Epstein D (22 July 2017). "When Evidence Says No, But Doctors Say Yes". The Atlantic . Archived from the original on 9 May 2018. Retrieved 8 May 2018.
  44. ↑ Choi HY, Oh IJ, Lee JA, Lim J, Kim YS, Jeon TH, et al. (November 2018). "Factors Affecting Adherence to Antihypertensive Medication". Korean Journal of Family Medicine. 39 (6): 325–332. doi:10.4082/kjfm.17.0041. PMC   6250947 . PMID   30384549.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.