Beta-adrenoceptors in cardiac disease

The human heart contains both β 1 and β- 2-adrenoceptors; both mediated positive inotropic and chronotropic effects. In chronic heart failure, β-adrenoceptor number is reduced, presumably, by down-regulation by endogenous noradrenaline which is elevated due to increased sympathetic activity. Since t...

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Published inPharmacology & therapeutics (Oxford) Vol. 60; no. 3; pp. 405 - 430
Main Author Brodde, Otto-Erich
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Inc 01.01.1993
Elsevier
Subjects
Adrenergic beta-Agonists - pharmacology
Adrenergic beta-Antagonists - pharmacology
Amino Acid Sequence
Biological and medical sciences
Cardiology. Vascular system
Down-Regulation
G-proteins
Heart
Heart - drug effects
Heart Diseases - metabolism
Heart Diseases - physiopathology
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Heart Transplantation
Human cardiac β1-adrenoceptors
human cardica β2-adrenoceptors chronic heart failure
Humans
Medical sciences
Molecular Sequence Data
Myocardial Contraction - drug effects
Receptors, Adrenergic, beta - chemistry
Receptors, Adrenergic, beta - drug effects
Receptors, Adrenergic, beta - physiology
β-adrenoceptor desensitization
PET, positron emission tomography
βARK, β-adrenoceptor kinase
PKC, protein kinase C
Human cardiac β 1-adrenoceptors
ACE, angiotensin-converting enzyme
human cardica β 2-adrenoceptors chronic heart failure
G-proteins
β-adrenoceptor desensitization
PKA, protein kinase A
Human
Heart failure
Pathophysiology
Contractility
Cyclic AMP
Cardiovascular disease
Review
Coronary heart disease
Myocardial disease
β-Adrenergic receptor
Vascular disease
Heart rate
Signal transduction
Ischemia
Heart disease
Myocardium
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Abstract The human heart contains both β 1 and β- 2-adrenoceptors; both mediated positive inotropic and chronotropic effects. In chronic heart failure, β-adrenoceptor number is reduced, presumably, by down-regulation by endogenous noradrenaline which is elevated due to increased sympathetic activity. Since the human heart contains only a few spare receptors for β-adrenoceptor-mediated positive inotropic effects and the amount of spare receptors declines in chronic heart failure, it is not surprising that the reduced β-adrenoceptor number is accompanied by decreased contractile responses to β-adrenoceptor agonists (including endogeneous catecholamines), and the extent of decrease in maximal inotropic response is more pronounced as the disease becomes more advanced. Moreover, in chronic heart failure myocardial G i-protein, which inhibits cAMP formation, is increased, which might further contribute to the reduction in β-adrenoceptor-mediated effects. It appears that, at present, the best therapy for severe heart failure is a successful heart transplant, since in the transplanted heart β-adrenoceptor number and function seems to be noramalized. Moreover, the data currently available do not suggest any development of super- or subsensitivity of postsynaptic cardiac β-adrenoceptors in the transplanted human heart.
AbstractList The human heart contains both beta 1 and beta 2-adrenoceptors; both mediate positive inotropic and chronotropic effects. In chronic heart failure, beta-adrenoceptor number is reduced, presumably, by down-regulation by endogenous noradrenaline which is elevated due to increased sympathetic activity. Since the human heart contains only a few spare receptors for beta-adrenoceptor-mediated positive inotropic effects and the amount of spare receptors declines in chronic heart failure, it is not surprising that the reduced beta-adrenoceptor number is accompanied by decreased contractile responses to beta-adrenoceptor agonists (including endogenous catecholamines), and the extent of decrease in maximal inotropic response is more pronounced as the disease becomes more advanced. Moreover, in chronic heart failure myocardial G(i)-protein, which inhibits cAMP formation, is increased, which might further contribute to the reduction in beta-adrenoceptor-mediated effects. It appears that, at present, the best therapy for severe heart failure is a successful heart transplant, since in the transplanted heart beta-adrenoceptor number and function seems to be normalized. Moreover, the data currently available do not suggest any development of super- or subsensitivity of postsynaptic cardiac beta-adrenoceptors in the transplanted human heart.
The human heart contains both β 1 and β- 2-adrenoceptors; both mediated positive inotropic and chronotropic effects. In chronic heart failure, β-adrenoceptor number is reduced, presumably, by down-regulation by endogenous noradrenaline which is elevated due to increased sympathetic activity. Since the human heart contains only a few spare receptors for β-adrenoceptor-mediated positive inotropic effects and the amount of spare receptors declines in chronic heart failure, it is not surprising that the reduced β-adrenoceptor number is accompanied by decreased contractile responses to β-adrenoceptor agonists (including endogeneous catecholamines), and the extent of decrease in maximal inotropic response is more pronounced as the disease becomes more advanced. Moreover, in chronic heart failure myocardial G i-protein, which inhibits cAMP formation, is increased, which might further contribute to the reduction in β-adrenoceptor-mediated effects. It appears that, at present, the best therapy for severe heart failure is a successful heart transplant, since in the transplanted heart β-adrenoceptor number and function seems to be noramalized. Moreover, the data currently available do not suggest any development of super- or subsensitivity of postsynaptic cardiac β-adrenoceptors in the transplanted human heart.
Author Brodde, Otto-Erich
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https://www.ncbi.nlm.nih.gov/pubmed/7915424$$D View this record in MEDLINE/PubMed
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CITATION
7X8
ID FETCH-LOGICAL-c437t-b9d84f3cc23caea4aa807890e35f0fb525d408bccadd84071f502f30220c94a63
ISSN 0163-7258
IngestDate Sat Aug 17 00:11:02 EDT 2024
Thu Sep 26 18:20:37 EDT 2024
Sat Sep 28 08:36:58 EDT 2024
Sun Oct 29 17:09:45 EDT 2023
Fri Feb 23 02:28:28 EST 2024
IsPeerReviewed true
IsScholarly true
Issue 3
Keywords PET, positron emission tomography
βARK, β-adrenoceptor kinase
PKC, protein kinase C
Human cardiac β 1-adrenoceptors
ACE, angiotensin-converting enzyme
human cardica β 2-adrenoceptors chronic heart failure
G-proteins
β-adrenoceptor desensitization
PKA, protein kinase A
Human
Heart failure
Pathophysiology
Contractility
Cyclic AMP
Cardiovascular disease
Review
Coronary heart disease
Myocardial disease
β-Adrenergic receptor
Vascular disease
Heart rate
Signal transduction
Ischemia
Heart disease
Myocardium
Language English
License CC BY 4.0
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c437t-b9d84f3cc23caea4aa807890e35f0fb525d408bccadd84071f502f30220c94a63
Notes ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
PMID 7915424
PQID 76290967
PQPubID 23479
PageCount 26
ParticipantIDs proquest_miscellaneous_76290967
crossref_primary_10_1016_0163_7258_93_90030_H
pubmed_primary_7915424
pascalfrancis_primary_4112470
elsevier_sciencedirect_doi_10_1016_0163_7258_93_90030_H
PublicationCentury 1900
PublicationDate 1993-01-01
PublicationDateYYYYMMDD 1993-01-01
PublicationDate_xml – month: 01
  year: 1993
  text: 1993-01-01
  day: 01
PublicationDecade 1990
PublicationPlace Amsterdam
PublicationPlace_xml – name: Amsterdam
– name: England
PublicationTitle Pharmacology & therapeutics (Oxford)
PublicationTitleAlternate Pharmacol Ther
PublicationYear 1993
Publisher Elsevier Inc
Elsevier
Publisher_xml – name: Elsevier Inc
– name: Elsevier
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SecondaryResourceType review_article
Snippet The human heart contains both β 1 and β- 2-adrenoceptors; both mediated positive inotropic and chronotropic effects. In chronic heart failure, β-adrenoceptor...
The human heart contains both beta 1 and beta 2-adrenoceptors; both mediate positive inotropic and chronotropic effects. In chronic heart failure,...
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SubjectTerms Adrenergic beta-Agonists - pharmacology
Adrenergic beta-Antagonists - pharmacology
Amino Acid Sequence
Biological and medical sciences
Cardiology. Vascular system
Down-Regulation
G-proteins
Heart
Heart - drug effects
Heart Diseases - metabolism
Heart Diseases - physiopathology
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Heart Transplantation
Human cardiac β1-adrenoceptors
human cardica β2-adrenoceptors chronic heart failure
Humans
Medical sciences
Molecular Sequence Data
Myocardial Contraction - drug effects
Receptors, Adrenergic, beta - chemistry
Receptors, Adrenergic, beta - drug effects
Receptors, Adrenergic, beta - physiology
β-adrenoceptor desensitization
Title Beta-adrenoceptors in cardiac disease
URI https://dx.doi.org/10.1016/0163-7258(93)90030-H
https://www.ncbi.nlm.nih.gov/pubmed/7915424
https://search.proquest.com/docview/76290967
Volume 60
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