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RESEARCH PRODUCT

Cardiac and vascular alpha(1)-adrenoceptors in congestive heart failure: a systematic review

Martin C. MichelA.h. Jan DanserMeindert PalmenGizem Kayki-mutluOlga PapazisiEbru Arioglu-inan

subject

0301 basic medicinemedicine.medical_specialtyα1-adrenoceptorsα(1)-adrenoceptorsmedicine.medical_treatmentheart failurecardiomyocyteReview030204 cardiovascular system & hematologyModels Biological03 medical and health sciences0302 clinical medicineDownregulation and upregulationblood vesselInternal medicineReceptors Adrenergic alpha-1medicineHumanslcsh:QH301-705.5Desensitization (medicine)business.industryMyocardiumα<sub>1</sub>-adrenoceptorsGeneral Medicinemedicine.diseaseα1 adrenoceptor030104 developmental biologySystematic reviewmedicine.anatomical_structurelcsh:Biology (General)Heart failureCardiologyBlood VesselsbusinessBlood vesselSignal Transduction

description

As heart failure (HF) is a devastating health problem worldwide, a better understanding and the development of more effective therapeutic approaches are required. HF is characterized by sympathetic system activation which stimulates α- and β-adrenoceptors (ARs). The exposure of the cardiovascular system to the increased locally released and circulating levels of catecholamines leads to a well-described downregulation and desensitization of β-ARs. However, information on the role of α-AR is limited. We have performed a systematic literature review examining the role of both cardiac and vascular α1-ARs in HF using 5 databases for our search. All three α1-AR subtypes (α1A, α1B and α1D) are expressed in human and animal hearts and blood vessels in a tissue-dependent manner. We summarize the changes observed in HF regarding the density, signaling and responses of α1-ARs. Conflicting findings arise from different studies concerning the influence that HF has on α1-AR expression and function; in contrast to β-ARs there is no consistent evidence for down-regulation or desensitization of cardiac or vascular α1-ARs. Whether α1-ARs are a therapeutic target in HF remains a matter of debate.

https://hdl.handle.net/1887/3184003