Jump to content

Atenolol

From Wikipedia, the free encyclopedia

Atenolol
Clinical data
Trade namesTenormin, others
Other namesICI-66082; ICI66082
AHFS/Drugs.comMonograph
MedlinePlusa684031
License data
Pregnancy
category
  • AU: C
Routes of
administration		Oral, intravenous
Drug classSelective β1 receptor antagonist
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • US: WARNING[1]
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability50–60%[2][3]
Protein binding6–16%[4]
MetabolismMinimal (~5%)[4][5][6]
Metabolites• Hydroxyatenolol[3]
• Atenolol glucuronide[3]
Onset of actionIVTooltip Intravenous injection: <5 minutes[4]
Oral: <1 hour[4]
Elimination half-life6–7 hours[4]
Duration of action>24 hours[4]
ExcretionOral: urine (40–50%), feces (50%)[3][4]
IVTooltip Intravenous injection: urine (85–100%), feces (10%)[3][4]
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 InfoCard100.044.941 Edit this at Wikidata
Chemical and physical data
FormulaC14H22N2O3
Molar mass266.341 g·mol−1
3D model (JSmol)
ChiralityRacemic 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) checkY
  • Key:METKIMKYRPQLGS-UHFFFAOYSA-N checkY
  (verify)

Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain.[7] Although used to treat high blood pressure, it does not seem to improve mortality in those with the condition.[8][9] Other uses include the prevention of migraines and treatment of certain irregular heart beats.[7][10] It is taken orally (by mouth) or by intravenous injection (injection into a vein).[7][10] It can also be used with other blood pressure medications.[10]

Common side effects include feeling tired, heart failure, dizziness, depression, and shortness of breath.[7] Other serious side effects include bronchial spasm.[7] Use is not recommended during pregnancy[7] and alternative drugs are preferred when breastfeeding.[11] It works by blocking β1-adrenergic receptors in the heart, thus decreasing heart rate, force of heart beats, and blood pressure.[7]

Atenolol was patented in 1969 and approved for medical use in 1975.[12] It is on the World Health Organization's List of Essential Medicines.[13] It is available as a generic medication.[7] In 2022, it was the 63rd most commonly prescribed medication in the United States, with more than 10 million prescriptions.[14][15]

Medical uses

[edit]

Atenolol is used for a number of conditions including hyperthyroidism,[16] hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, and the symptoms of alcohol withdrawal.[17]

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.[18][19][20]

Available forms

[edit]

Atenolol is available in the form of 25, 50, and 100 mg oral tablets.[21][4] It is also available in the form of oral tablets containing a combination of 50 or 100 mg atenolol and 50 mg chlortalidone.[21] Atenolol was previously available in a 0.5 mg/mL solution for injection as well, but this formulation was discontinued.[21]

Side effects

[edit]
See also: Beta blocker

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.[22][23]

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.[24][25][26][18] Diuretics may be associated with better cardiovascular and cerebrovascular outcomes than β-blockers in the elderly.[27]

Rarely, atenolol has been associated with induction of acute delirium.[28][2][29]

Overdose

[edit]

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.[30][31]

Interactions

[edit]

Interactions with atenolol include catecholamine-depleting drugs like reserpine, calcium channel blockers, disopyramide, amiodarone, clonidine, prostaglandin synthase inhibitors like indomethacin, and digitalis glycosides.[32] Most of these interactions involve either additive cardiovascular effects or reduction of atenolol's effects.[32]

Atenolol is mainly eliminated renally without being metabolized by the liver or by cytochrome P450 enzymes.[32][5][33] As a result, it has little or no potential for cytochrome P450-related drug interactions, for instance with inhibitors and inducers of these enzymes.[5][33] Accordingly, the broad/non-selective cytochrome P450 inhibitor cimetidine had no effect on atenolol levels, whereas cimetidine has been found to significantly increase metoprolol and propranolol levels.[5]

Beta blockers like atenolol can reduce or block the cardiovascular effects of sympathomimetics and amphetamines, such as hypertension and tachycardia.[34][35][36][37][38][39][40]

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.[41][42][43] 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.[41][43]

Pharmacology

[edit]

Pharmacodynamics

[edit]

Atenolol is a beta blocker; that is, an antagonist of the β-adrenergic receptors.[44][4] 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.[44][4] However, the preferential action of atenolol is not absolute, and at high doses, it can also block β2-adrenergic receptors.[4]

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 of tachycardia induced by isoproterenol (a non-selective β-adrenergic receptor agonist), and reduction of reflex orthostatic tachycardia.[4]

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.[4] The general effects of atenolol, including beta-blocking and antihypertensive effects, last for at least 24 hours following oral doses of 50 or 100 mg.[4] 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.[4] The duration of action of atenolol is dose-related and is correlated with circulating levels of atenolol.[4]

Pharmacokinetics

[edit]

Absorption

[edit]

The oral bioavailability of atenolol is approximately 50 to 60%.[2][3] The absorption of atenolol with oral administration is rapid and consistent but is incomplete.[4] About 50% of an oral dose of atenolol is absorbed from the intestines, with the rest excreted in feces.[4] Maximal concentrations of atenolol occur 2 to 4 hours following an oral dose, whereas peak concentrations occur within 5 minutes with intravenous administration.[4] The pharmacokinetic profile of atenolol results in it having relatively consistent plasma drug levels with about 4-fold variation between individuals.[4]

Distribution

[edit]

The plasma protein binding of atenolol is 6 to 16%.[4]

Atenolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier and entering the brain.[44] This in turn may result in fewer effects in the central nervous system as well as a lower risk of neuropsychiatric side effects.[44] Only small amounts of atenolol are said to enter the brain.[2][3] The brain-to-blood ratio of atenolol was 0.2 : 1 in one study, whereas the ratio for propranolol was 33 : 1 in the same study.[3]

Metabolism

[edit]

Atenolol undergoes minimal or negligible metabolism by the liver.[4][5] It has been estimated that about 5% of atenolol is metabolized.[6] This is in contrast to other beta blockers like propranolol and metoprolol, but is similar to nadolol.[4] In accordance with its lack of hepatic metabolism, the pharmacokinetics of atenolol are not altered in hepatic impairment, unlike the case of propranolol.[5] Two metabolites of atenolol have been identified: hydroxyatenolol and atenolol glucuronide.[2] It has been said that it is unknown if these metabolites are active.[2] However, another source stated that hydroxyatenolol has one-tenth the beta-blocking activity of atenolol.[3]

Elimination

[edit]

Instead of by hepatic metabolism, atenolol is eliminated from the blood mainly via renal excretion.[4] Atenolol is excreted about 40 to 50% in urine and 50% in feces with oral administration.[3][4] Conversely, it is excreted 85 to 100% in urine unchanged and 10% in feces with intravenous administration.[3][4] Only very small amounts of hydroxyatenolol and atenolol glucuronide are found in urine with atenolol.[3]

The elimination half-life of atenolol is about 6 to 7 hours.[4] The half-life of atenolol does not change with continuous administration.[4] 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.[4]

The elimination of atenolol is slowed in renal impairment, with the elimination rate being closely related to the glomerular filtration rate (GFR) and with significant accumulation occurring when the creatinine clearance rate is under 35 mL/min/1.73 m2.[4] At a GFR of less than 10 mL/min, the half-life of atenolol increases up to 36 hours.[6]

Chemistry

[edit]

Atenolol is a substituted phenethylamine derivative.[45] It is specifically β-phenylethylamine with an α-keto substitution and a 4- substitution on the phenyl ring.[45]

The experimental log P of atenolol is 0.16 and its predicted log P ranges from −0.03 to 0.57.[45][46][47]

Atenolol is closely structurally related to metoprolol and certain other beta blockers. It is also structurally related to the catecholamine neurotransmitters epinephrine (adrenaline) and norepinephrine (noradrenaline).

Society and culture

[edit]

Changing medical practices

[edit]

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.[48] In 2012, 33.8 million prescriptions were written to American patients for this drug.[48] In 2014, it was in the top (most common) 1% of drugs prescribed to Medicare patients.[48] 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.[48] 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.[18] 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.[49]

References

[edit]
  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. ^ a b c d e f Wadworth AN, Murdoch D, Brogden RN (September 1991). "Atenolol. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disorders". Drugs. 42 (3): 468–510. doi:10.2165/00003495-199142030-00007. PMID 1720383.
  3. ^ a b c d e f g h i j k l Heel RC, Brogden RN, Speight TM, Avery GS (June 1979). "Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension". Drugs. 17 (6): 425–460. doi:10.2165/00003495-197917060-00001. PMID 38096.
  4. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae "DailyMed - TENORMIN- atenolol tablet". DailyMed. 30 June 2021. Archived from the original on 27 January 2022. Retrieved 20 November 2023.
  5. ^ a b c d e f 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).
  6. ^ a b c Kirch W, Görg KG (1982). "Clinical pharmacokinetics of atenolol--a review". Eur J Drug Metab Pharmacokinet. 7 (2): 81–91. doi:10.1007/BF03188723. PMID 6749509.
  7. ^ a b c d e f g h "Atenolol Monograph for Professionals". Drugs.com. AHFS. Archived from the original on 18 April 2019. Retrieved 23 December 2018.
  8. ^ 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.
  9. ^ 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.
  10. ^ a b c British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. pp. 151–153. ISBN 9780857113382.
  11. ^ "Atenolol use while Breastfeeding". Drugs.com. Archived from the original on 23 December 2018. Retrieved 23 December 2018.
  12. ^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 461. ISBN 9783527607495.
  13. ^ 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.
  14. ^ "The Top 300 of 2022". ClinCalc. Archived from the original on 30 August 2024. Retrieved 30 August 2024.
  15. ^ "Atenolol Drug Usage Statistics, United States, 2013 - 2022". ClinCalc. Retrieved 30 August 2024.
  16. ^ 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.
  17. ^ "Atenolol". The American Society of Health-System Pharmacists. Archived from the original on 18 April 2019. Retrieved 8 May 2018.
  18. ^ a b c 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)
  19. ^ 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.
  20. ^ 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.
  21. ^ a b c "Drugs@FDA: FDA-Approved Drugs". accessdata.fda.gov. Retrieved 8 July 2024.
  22. ^ 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.
  23. ^ 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.
  24. ^ 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.
  25. ^ 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.
  26. ^ 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.
  27. ^ 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.
  28. ^ Keller S, Frishman WH (2003). "Neuropsychiatric effects of cardiovascular drug therapy". Cardiol Rev. 11 (2): 73–93. doi:10.1097/01.CRD.0000053453.89776.2D. PMID 12620132.
  29. ^ Arber N (October 1988). "Delirium induced by atenolol". BMJ. 297 (6655): 1048. doi:10.1136/bmj.297.6655.1048-b. PMC 1834788. PMID 3142623.
  30. ^ 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.
  31. ^ Baselt R (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, Calif.: Biomedical Publications. pp. 116–117.
  32. ^ a b c "TENORMIN® (atenolol) Tablets Drug Label" (PDF). Food and Drug Administration. December 2023. Retrieved 8 July 2024.
  33. ^ a b 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].
  34. ^ 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.
  35. ^ 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
  36. ^ 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.
  37. ^ 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.
  38. ^ 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.
  39. ^ 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. doi:10.1002/j.1875-9114.1990.tb02554.x. PMID 2349137.
  40. ^ 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. doi:10.1002/j.1875-9114.1991.tb02648.x. PMID 1684039.
  41. ^ a b 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.
  42. ^ 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).
  43. ^ a b 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.
  44. ^ a b c d 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.
  45. ^ a b c "Atenolol". PubChem. Retrieved 1 August 2024.
  46. ^ "Atenolol: Uses, Interactions, Mechanism of Action". DrugBank Online. 13 August 2004. Retrieved 1 August 2024.
  47. ^ "DL-Atenolol". ChemSpider. 21 July 2022. Retrieved 1 August 2024.
  48. ^ a b c d 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.
  49. ^ 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.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Atenolol&oldid=1260744767"
pFad - Phonifier reborn

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.

Note: This service is not intended for secure transactions such as banking, social media, email, or purchasing. Use at your own risk. We assume no liability whatsoever for broken pages.


Alternative Proxies:

Alternative Proxy

pFad Proxy

pFad v3 Proxy

pFad v4 Proxy