Jump to content

Isoprenaline: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
No edit summary
reformatted refs
Line 55: Line 55:


==Medical uses==
==Medical uses==
It is used to treat [[heart block]] and episodes of [[Adams–Stokes syndrome]] that are not caused by [[ventricular tachycardia]] or fibrillation, in emergencies for [[cardiac arrest]] until electric shock can be administered, for bronchospasm occurring during anesthesia, and as an adjunct in the treatment of [[hypovolemic shock]], [[septic shock]], low cardiac output (hypoperfusion) states, congestive heart failure, and cardiogenic shock.<ref name=USlabel2013/> It is also used to prevent [[Torsades de Pointes]] in patients with [[long QT]] refractory to magnesium and to treat patients with intermittent Torsades de Pointes refractory to treatment with magnesium.<ref name=Cohagan2022>{{cite book | vauthors = Cohagan B, Brandis D | chapter = Torsade de Pointes | date = August 2022 | title = StatPearls | location = Treasure Island (FL) | publisher = StatPearls Publishing | chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK459388/}}</ref>
It is used to treat [[heart block]] and episodes of [[Adams–Stokes syndrome]] that are not caused by [[ventricular tachycardia]] or fibrillation, in emergencies for [[cardiac arrest]] until electric shock can be administered, for bronchospasm occurring during anesthesia, and as an adjunct in the treatment of [[hypovolemic shock]], [[septic shock]], low cardiac output (hypoperfusion) states, congestive heart failure, and cardiogenic shock.<ref name=USlabel2013/> It is also used to prevent [[Torsades de Pointes]] in patients with [[long QT]] refractory to magnesium and to treat patients with intermittent Torsades de Pointes refractory to treatment with magnesium.<ref name=Cohagan2022>{{cite book | vauthors = Cohagan B, Brandis D | chapter = Torsade de Pointes | date = August 2022 | title = StatPearls | location = Treasure Island (FL) | publisher = StatPearls Publishing |id={{NCBIBook2|NBK459388}} |pmid=29083738 }}</ref>


Historically, it was used to treat asthma via metered aerosol or nebulizing devices; it was also available in sublingual, oral, intravenous, and intramuscular formulations.<ref name=Mozayan2003book/> The U.S. National Asthma Education and Prevention Program Expert Panel recommends against its use as a nebulizer for acute bronchoconstriction.<ref>{{cite web|last1=National Asthma Education and Prevention Program Expert Panel |title= Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma |url= https://www.nhlbi.nih.gov/files/docs/guidelines/asthgdln.pdf |publisher=NIH National Heart, Lung, and Blood Institute|date=August 28, 2007}}</ref>
Historically, it was used to treat asthma via metered aerosol or nebulizing devices; it was also available in sublingual, oral, intravenous, and intramuscular formulations.<ref name=Mozayan2003book/> The U.S. National Asthma Education and Prevention Program Expert Panel recommends against its use as a nebulizer for acute bronchoconstriction.<ref>{{cite web|last1=National Asthma Education and Prevention Program Expert Panel |title= Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma |url= https://www.nhlbi.nih.gov/files/docs/guidelines/asthgdln.pdf |publisher=NIH National Heart, Lung, and Blood Institute|date=August 28, 2007}}</ref>
Line 71: Line 71:


===Pharmacodynamics===
===Pharmacodynamics===
Isoprenaline is a [[Beta-1 adrenergic receptor|β<sub>1</sub>]] and [[Beta-2 adrenergic receptor|β<sub>2</sub>]] adrenoreceptor agonist and has almost no activity on [[alpha adrenergic receptor]]s at low levels.<ref name=Mozayan2003book/> However, at higher concentrations, isoprenaline can evoke α-AR-mediated responses.<ref>https://pubmed.ncbi.nlm.nih.gov/13062084/</ref><ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4301629/?fbclid=IwAR0U44Tg8xUojyhmblh4i8a2ApCJ0dAhBS8M23l5b8hQArK-r-0X3r8bkoA#pone.0115701.ref009</ref> Its agonist effects at [[TAAR1]] provide it with pharmacodynamic effects that resemble those of the endogenous [[trace amine]]s, like [[tyramine]].<ref name="TAAR1 ligands and TA adrenergic receptor binding">{{cite journal | vauthors = Kleinau G, Pratzka J, Nürnberg D, Grüters A, Führer-Sakel D, Krude H, Köhrle J, Schöneberg T, Biebermann H | display-authors = 6 | title = Differential modulation of Beta-adrenergic receptor signaling by trace amine-associated receptor 1 agonists | journal = PLOS ONE | volume = 6 | issue = 10 | pages = e27073 | date = October 2011 | pmid = 22073124 | pmc = 3205048 | doi = 10.1371/journal.pone.0027073 | doi-access = free | bibcode = 2011PLoSO...627073K }}<br />"[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3205048/table/pone-0027073-t001/ Table 1: EC<sub>50</sub> values of different agonists at hTAAR1, hADRB1 and hADRB2.]"</ref>
Isoprenaline is a [[Beta-1 adrenergic receptor|β<sub>1</sub>]] and [[Beta-2 adrenergic receptor|β<sub>2</sub>]] adrenoreceptor agonist and has almost no activity on [[alpha adrenergic receptor]]s at low levels.<ref name=Mozayan2003book/> However, at higher concentrations, isoprenaline can evoke α-AR-mediated responses.<ref>{{cite journal |last1=Furchgott |first1=Robert F. |last2=Bhadrakom |first2=Suchin |title=Reactions of strips of rabbit aorta to epinephrine, isopropylarterenol, sodium nitrite and other drugs |journal=The Journal of Pharmacology and Experimental Therapeutics |date=June 1953 |volume=108 |issue=2 |pages=129–143 |pmid=13062084 |url=https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13062084 }}</ref><ref>{{cite journal |last1=Copik |first1=Alicja. J. |last2=Baldys |first2=Aleksander |last3=Nguyen |first3=Khanh |last4=Sahdeo |first4=Sunil |last5=Ho |first5=Hoangdung |last6=Kosaka |first6=Alan |last7=Dietrich |first7=Paul J. |last8=Fitch |first8=Bill |last9=Raymond |first9=John R. |last10=Ford |first10=Anthony P. D. W. |last11=Button |first11=Donald |last12=Milla |first12=Marcos E. |title=Isoproterenol Acts as a Biased Agonist of the Alpha-1A-Adrenoceptor that Selectively Activates the MAPK/ERK Pathway |journal=PLOS ONE |date=21 January 2015 |volume=10 |issue=1 |pages=e0115701 |doi=10.1371/journal.pone.0115701 |pmid=25606852 |pmc=4301629 }}</ref> Its agonist effects at [[TAAR1]] provide it with pharmacodynamic effects that resemble those of the endogenous [[trace amine]]s, like [[tyramine]].<ref name="TAAR1 ligands and TA adrenergic receptor binding">{{cite document |doi=10.1371/journal.pone.0027073.t001 |doi-access=free |title=Table 1. EC50 values of different agonists at hTAAR1, hADRB1 and hADRB2 }} in {{cite journal | vauthors = Kleinau G, Pratzka J, Nürnberg D, Grüters A, Führer-Sakel D, Krude H, Köhrle J, Schöneberg T, Biebermann H | display-authors = 6 | title = Differential modulation of Beta-adrenergic receptor signaling by trace amine-associated receptor 1 agonists | journal = PLOS ONE | volume = 6 | issue = 10 | pages = e27073 | date = October 2011 | pmid = 22073124 | pmc = 3205048 | doi = 10.1371/journal.pone.0027073 | doi-access = free | bibcode = 2011PLoSO...627073K }}</ref>


Isoprenaline's effects on the [[cardiovascular system]] (non-selective) relate to its actions on cardiac β<sub>1</sub> receptors and β<sub>2</sub> receptors on smooth muscle within the [[tunica media]] of [[arteriole]]s. Isoprenaline has positive inotropic and [[chronotropic]] effects on the heart. β<sub>2</sub> adrenoceptor stimulation in arteriolar smooth muscle induces vasodilation. Its inotropic and chronotropic effects elevate [[Systole|systolic]] [[blood pressure]], while its vasodilatory effects tend to lower [[Diastole|diastolic]] blood pressure. The overall effect is to decrease [[mean arterial pressure]] due to the β<sub>2</sub> receptors' vasodilation.<ref>{{cite book| vauthors = Korbut R |title=Farmakologia|date=2017|publisher=Wydawnictwo Lekarskie PZWL|isbn=9788320053685|pages=36|language=pl}}</ref>
Isoprenaline's effects on the [[cardiovascular system]] (non-selective) relate to its actions on cardiac β<sub>1</sub> receptors and β<sub>2</sub> receptors on smooth muscle within the [[tunica media]] of [[arteriole]]s. Isoprenaline has positive inotropic and [[chronotropic]] effects on the heart. β<sub>2</sub> adrenoceptor stimulation in arteriolar smooth muscle induces vasodilation. Its inotropic and chronotropic effects elevate [[Systole|systolic]] [[blood pressure]], while its vasodilatory effects tend to lower [[Diastole|diastolic]] blood pressure. The overall effect is to decrease [[mean arterial pressure]] due to the β<sub>2</sub> receptors' vasodilation.<ref>{{cite book| vauthors = Korbut R |title=Farmakologia|date=2017|publisher=Wydawnictwo Lekarskie PZWL|isbn=978-83-200-5368-5|page=36|language=pl}}</ref>


The [[isopropylamine]] group in isoprenaline makes it selective for β receptors. The free [[catechol]] [[hydroxyl]] groups keep it susceptible to enzymatic metabolism.<ref>{{cite web| vauthors = Mehta A |title=Notes - Medicinal Chemistry of the Peripheral Nervous System - Adrenergics and Cholinergic |url= http://pharmaxchange.info/notes/medicinal_chemistry/adrenergics_cholinergics.html |publisher=Pharmaxchange |access-date=June 21, 2017 |date=January 27, 2011|archive-url= https://web.archive.org/web/20101104022742/http://pharmaxchange.info/notes/medicinal_chemistry/adrenergics_cholinergics.html|archive-date=4 November 2010|url-status=dead}}</ref>
The [[isopropylamine]] group in isoprenaline makes it selective for β receptors. The free [[catechol]] [[hydroxyl]] groups keep it susceptible to enzymatic metabolism.<ref>{{cite web| vauthors = Mehta A |title=Notes - Medicinal Chemistry of the Peripheral Nervous System - Adrenergics and Cholinergic |url= http://pharmaxchange.info/notes/medicinal_chemistry/adrenergics_cholinergics.html |publisher=Pharmaxchange |access-date=June 21, 2017 |date=January 27, 2011|archive-url= https://web.archive.org/web/20101104022742/http://pharmaxchange.info/notes/medicinal_chemistry/adrenergics_cholinergics.html|archive-date=4 November 2010|url-status=dead}}</ref>


===Pharmacokinetics===
===Pharmacokinetics===
The plasma half-life for isoproterenol is approximately two to five minutes. It is degraded enzymatically via catechol O-methyltransferase (COMT) primarily in the liver and excreted in the urine as sulfated conjugates.<ref>David E. Procaccini, Jaclyn E. Sawyer, Kevin M. Watt,
The plasma half-life for isoproterenol is approximately two to five minutes. It is degraded enzymatically via catechol O-methyltransferase (COMT) primarily in the liver and excreted in the urine as sulfated conjugates.<ref>{{cite journal |doi=10.1016/B978-1-4557-0760-7.00019-X }}</ref><ref name=Szymanski2022>{{cite book |last1=Szymanski |first1=Michael W. |last2=Singh |first2=Davinder P. |chapter=Isoproterenol |title=StatPearls |date=2023 |publisher=StatPearls Publishing |id={{NCBIBook2|NBK526042}} |pmid=30252298 }}</ref>
19 - Pharmacology of Cardiovascular Drugs,
Editor(s): Ross M. Ungerleider, Jon N. Meliones, Kristen Nelson McMillan, David S. Cooper, Jeffrey P. Jacobs,
Critical Heart Disease in Infants and Children (Third Edition),
Elsevier,
2019,
Pages 192-212.e6,
ISBN 9781455707607,
https://doi.org/10.1016/B978-1-4557-0760-7.00019-X.
(https://www.sciencedirect.com/science/article/pii/B978145570760700019X)
</ref><ref name=Szymanski2022>Szymanski MW, Singh DP. Isoproterenol. [Updated 2022 Sep 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526042/</ref>


==Chemistry==
==Chemistry==
Line 94: Line 84:


==History==
==History==
It was first approved in the US in 1947.<ref name=Mozayan2003book>{{cite book| vauthors = Mozayani A, Raymon L |title=Handbook of Drug Interactions: A Clinical and Forensic Guide|date=2003|publisher=Springer Science & Business Media|isbn=9781592596546|pages=541–542|url=https://books.google.com/books?id=dwMyBwAAQBAJ&pg=PA541|language=en}}</ref>
It was first approved in the US in 1947.<ref name=Mozayan2003book>{{cite book| vauthors = Mozayani A, Raymon L |title=Handbook of Drug Interactions: A Clinical and Forensic Guide|date=2003|publisher=Springer Science & Business Media|isbn=978-1-59259-654-6|pages=541–542|url=https://books.google.com/books?id=dwMyBwAAQBAJ&pg=PA541|language=en}}</ref>
Between 1963 and 1968 in England, Wales, Scotland, Ireland, Australia, and New Zealand there was an increase in deaths among people using isoprenaline to treat asthma. This was attributed to overdose: the inhalers produced in that area were dispensing five times the dosage dispensed by inhalers produced in the US and Canada, where the deaths were not observed.<ref>{{cite journal | vauthors = Pearce N, Hensley MJ | title = Epidemiologic studies of beta agonists and asthma deaths | journal = Epidemiologic Reviews | volume = 20 | issue = 2 | pages = 173–186 | year = 1998 | pmid = 9919437 | doi = 10.1093/oxfordjournals.epirev.a017979 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Jalba MS | title = Three generations of ongoing controversies concerning the use of short acting beta-agonist therapy in asthma: a review | journal = The Journal of Asthma | volume = 45 | issue = 1 | pages = 9–18 | date = 2008 | pmid = 18259990 | doi = 10.1080/02770900701495512 | s2cid = 31732029 }}</ref>
Between 1963 and 1968 in England, Wales, Scotland, Ireland, Australia, and New Zealand there was an increase in deaths among people using isoprenaline to treat asthma. This was attributed to overdose: the inhalers produced in that area were dispensing five times the dosage dispensed by inhalers produced in the US and Canada, where the deaths were not observed.<ref>{{cite journal | vauthors = Pearce N, Hensley MJ | title = Epidemiologic studies of beta agonists and asthma deaths | journal = Epidemiologic Reviews | volume = 20 | issue = 2 | pages = 173–186 | year = 1998 | pmid = 9919437 | doi = 10.1093/oxfordjournals.epirev.a017979 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Jalba MS | title = Three generations of ongoing controversies concerning the use of short acting beta-agonist therapy in asthma: a review | journal = The Journal of Asthma | volume = 45 | issue = 1 | pages = 9–18 | date = 2008 | pmid = 18259990 | doi = 10.1080/02770900701495512 | s2cid = 31732029 }}</ref>


Revision as of 19:52, 13 July 2023

Isoprenaline
INN: Isoprenaline
Clinical data
Trade namesMany[1]
Other namesIsoproterenol (USAN US)
MedlinePlusa601236
Pregnancy
category
  • AU: A
Routes of
administration		Inhalation (80–120 μg), intravenous injection (IV)
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Elimination half-life~2 minutes
Identifiers
  • (RS)-4-[1-hydroxy-2-(isopropylamino)ethyl]benzene-1,2-diol
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.028.807 Edit this at Wikidata
Chemical and physical data
FormulaC11H17NO3
Molar mass211.261 g·mol−1
3D model (JSmol)
  • CC(C)NCC(O)c1cc(O)c(O)cc1
  • InChI=1S/C11H17NO3/c1-7(2)12-6-11(15)8-3-4-9(13)10(14)5-8/h3-5,7,11-15H,6H2,1-2H3 checkY
  • Key:JWZZKOKVBUJMES-UHFFFAOYSA-N checkY
  (verify)

Isoprenaline, or isoproterenol (brand name: Isoprenaline Macure), is a medication used for the treatment of bradycardia (slow heart rate), heart block, and rarely for asthma. It is a non-selective β adrenoceptor agonist that is the isopropylamine analog of epinephrine (adrenaline).[2]

Medical uses

It is used to treat heart block and episodes of Adams–Stokes syndrome that are not caused by ventricular tachycardia or fibrillation, in emergencies for cardiac arrest until electric shock can be administered, for bronchospasm occurring during anesthesia, and as an adjunct in the treatment of hypovolemic shock, septic shock, low cardiac output (hypoperfusion) states, congestive heart failure, and cardiogenic shock.[2] It is also used to prevent Torsades de Pointes in patients with long QT refractory to magnesium and to treat patients with intermittent Torsades de Pointes refractory to treatment with magnesium.[3]

Historically, it was used to treat asthma via metered aerosol or nebulizing devices; it was also available in sublingual, oral, intravenous, and intramuscular formulations.[4] The U.S. National Asthma Education and Prevention Program Expert Panel recommends against its use as a nebulizer for acute bronchoconstriction.[5]

Isoprenaline can also ameliorate the impairment of intestinal stem cells mediated by β2-adrenoreceptors after chemotherapy.[6]

Contraindications

It should not be used in people with tachyarrhythmias (except in special circumstances),[7] tachycardia or heart block caused by digitalis poisoning, ventricular arrhythmias which require inotropic therapy, or with angina.[2]

Adverse effects

Adverse effects of isoprenaline include nervousness, headache, dizziness, nausea, visual blurring, tachycardia, palpitations, angina, Adams-Stokes attacks, pulmonary edema, hypertension, hypotension, ventricular arrhythmias, tachyarrhythmias, difficulty breathing, sweating, mild tremors, weakness, flushing, and pallor.[2] Isoproterenol has been reported to cause insulin resistance leading to diabetic ketoacidosis.[8]

Pharmacology

The adverse effects of isoprenaline are also related to the drug's cardiovascular effects. Isoprenaline can produce tachycardia (an elevated heart rate), which predisposes people who take it to cardiac arrhythmias.[4]

Pharmacodynamics

Isoprenaline is a β1 and β2 adrenoreceptor agonist and has almost no activity on alpha adrenergic receptors at low levels.[4] However, at higher concentrations, isoprenaline can evoke α-AR-mediated responses.[9][10] Its agonist effects at TAAR1 provide it with pharmacodynamic effects that resemble those of the endogenous trace amines, like tyramine.[11]

Isoprenaline's effects on the cardiovascular system (non-selective) relate to its actions on cardiac β1 receptors and β2 receptors on smooth muscle within the tunica media of arterioles. Isoprenaline has positive inotropic and chronotropic effects on the heart. β2 adrenoceptor stimulation in arteriolar smooth muscle induces vasodilation. Its inotropic and chronotropic effects elevate systolic blood pressure, while its vasodilatory effects tend to lower diastolic blood pressure. The overall effect is to decrease mean arterial pressure due to the β2 receptors' vasodilation.[12]

The isopropylamine group in isoprenaline makes it selective for β receptors. The free catechol hydroxyl groups keep it susceptible to enzymatic metabolism.[13]

Pharmacokinetics

The plasma half-life for isoproterenol is approximately two to five minutes. It is degraded enzymatically via catechol O-methyltransferase (COMT) primarily in the liver and excreted in the urine as sulfated conjugates.[14][15]

Chemistry

It is structurally related to epinephrine.[2]

History

It was first approved in the US in 1947.[4] Between 1963 and 1968 in England, Wales, Scotland, Ireland, Australia, and New Zealand there was an increase in deaths among people using isoprenaline to treat asthma. This was attributed to overdose: the inhalers produced in that area were dispensing five times the dosage dispensed by inhalers produced in the US and Canada, where the deaths were not observed.[16][17]

Society and culture

Brands

As of June 2017, isoprenaline was marketed under many brand names worldwide and as two different salts: Aleudrina, Asthpul, Iludrin, Isomenyl, Isoprenalin, Isoprenalina, Isoprenaline, Isoprénaline, Isoprenaline hydrochloride, Isoprenaline sulfate, Isoprenalinesulfaat, Isoprenalinsulfat, Isoprenalinum, Isopropydine, Isopropylnoradrenaline, Isoproterenol, Isoproterenol hydrochloride, Isoproterenol sulfate, Isuprel, Isuprel, Neo-Epinine, Neodrenal, Proternol, Saventrine, and Win 5162.[1] It is also marketed as a combination drug with cromoglicic acid as Frenal Compositum, in combination with pronase as Isopal P, and in combination with atropine as Stmerin D.[1]

References

  1. ^ a b c "Isoprenaline international brands". Drugs.com. Archived from the original on June 26, 2019. Retrieved June 21, 2017.
  2. ^ a b c d e "Label: Isoproterenol hydrochloride injection, solution". NIH DailyMed. September 10, 2013. Retrieved June 21, 2017.
  3. ^ Cohagan B, Brandis D (August 2022). "Torsade de Pointes". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 29083738. NBK459388.
  4. ^ a b c d Mozayani A, Raymon L (2003). Handbook of Drug Interactions: A Clinical and Forensic Guide. Springer Science & Business Media. pp. 541–542. ISBN 978-1-59259-654-6.
  5. ^ National Asthma Education and Prevention Program Expert Panel (August 28, 2007). "Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma" (PDF). NIH National Heart, Lung, and Blood Institute.
  6. ^ Zeng H, Li H, Yue M, Fan Y, Cheng J, Wu X, et al. (February 2020). "Isoprenaline protects intestinal stem cells from chemotherapy-induced damage". British Journal of Pharmacology. 177 (3): 687–700. doi:10.1111/bph.14883. PMC 7012967. PMID 31648381.
  7. ^ Jongman JK, Jepkes-Bruin N, Ramdat Misier AR, Beukema WP, Delnoy PP, Oude Lutttikhuis H, et al. (April 2007). "Electrical storms in Brugada syndrome successfully treated with isoproterenol infusion and quinidine orally". Netherlands Heart Journal. 15 (4): 151–155. doi:10.1007/BF03085972. PMC 1847769. PMID 17612676.
  8. ^ Hoff R, Koh CK (2018). "Isoproterenol Induced Insulin Resistance Leading to Diabetic Ketoacidosis in Type 1 Diabetes Mellitus". Case Reports in Endocrinology. 2018: 4328954. doi:10.1155/2018/4328954. PMC 6311779. PMID 30647979.
  9. ^ Furchgott, Robert F.; Bhadrakom, Suchin (June 1953). "Reactions of strips of rabbit aorta to epinephrine, isopropylarterenol, sodium nitrite and other drugs". The Journal of Pharmacology and Experimental Therapeutics. 108 (2): 129–143. PMID 13062084.
  10. ^ Copik, Alicja. J.; Baldys, Aleksander; Nguyen, Khanh; Sahdeo, Sunil; Ho, Hoangdung; Kosaka, Alan; Dietrich, Paul J.; Fitch, Bill; Raymond, John R.; Ford, Anthony P. D. W.; Button, Donald; Milla, Marcos E. (21 January 2015). "Isoproterenol Acts as a Biased Agonist of the Alpha-1A-Adrenoceptor that Selectively Activates the MAPK/ERK Pathway". PLOS ONE. 10 (1): e0115701. doi:10.1371/journal.pone.0115701. PMC 4301629. PMID 25606852.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ "Table 1. EC50 values of different agonists at hTAAR1, hADRB1 and hADRB2" (Document). doi:10.1371/journal.pone.0027073.t001. {{cite document}}: Cite document requires |publisher= (help) in Kleinau G, Pratzka J, Nürnberg D, Grüters A, Führer-Sakel D, Krude H, et al. (October 2011). "Differential modulation of Beta-adrenergic receptor signaling by trace amine-associated receptor 1 agonists". PLOS ONE. 6 (10): e27073. Bibcode:2011PLoSO...627073K. doi:10.1371/journal.pone.0027073. PMC 3205048. PMID 22073124.
  12. ^ Korbut R (2017). Farmakologia (in Polish). Wydawnictwo Lekarskie PZWL. p. 36. ISBN 978-83-200-5368-5.
  13. ^ Mehta A (January 27, 2011). "Notes - Medicinal Chemistry of the Peripheral Nervous System - Adrenergics and Cholinergic". Pharmaxchange. Archived from the original on 4 November 2010. Retrieved June 21, 2017.
  14. ^ . doi:10.1016/B978-1-4557-0760-7.00019-X. {{cite journal}}: Cite journal requires |journal= (help); Missing or empty |title= (help)
  15. ^ Szymanski, Michael W.; Singh, Davinder P. (2023). "Isoproterenol". StatPearls. StatPearls Publishing. PMID 30252298. NBK526042.
  16. ^ Pearce N, Hensley MJ (1998). "Epidemiologic studies of beta agonists and asthma deaths". Epidemiologic Reviews. 20 (2): 173–186. doi:10.1093/oxfordjournals.epirev.a017979. PMID 9919437.
  17. ^ Jalba MS (2008). "Three generations of ongoing controversies concerning the use of short acting beta-agonist therapy in asthma: a review". The Journal of Asthma. 45 (1): 9–18. doi:10.1080/02770900701495512. PMID 18259990. S2CID 31732029.
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Isoprenaline&oldid=1165223199"