Cardiac and Vascular alpha(1)-Adrenoceptors in Congestive Heart Failure: A Systematic Review

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KAYKI MUTLU G., Papazisi O., Palmen M., Danser A. H. J., Michel M. C., ARIOĞLU İNAN E.

CELLS, cilt.9, sa.11, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 9 Sayı: 11
  • Basım Tarihi: 2020
  • Doi Numarası: 10.3390/cells9112412
  • Dergi Adı: CELLS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, EMBASE, MEDLINE, Directory of Open Access Journals
  • Anahtar Kelimeler: &#945, (1)-adrenoceptors, cardiomyocyte, blood vessel, heart failure, ADRENOCEPTOR GENE-EXPRESSION, ALPHA-ADRENERGIC RECEPTORS, BLOOD-PRESSURE RESPONSE, SMOOTH-MUSCLE, ALPHA-1-ADRENERGIC RECEPTORS, RESISTANCE ARTERIES, MESSENGER-RNA, DILATED CARDIOMYOPATHY, MYOCARDIAL-INFARCTION, TISSUE DISTRIBUTION
  • Ankara Üniversitesi Adresli: Evet

Özet

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 alpha- and beta-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 beta-ARs. However, information on the role of alpha-AR is limited. We have performed a systematic literature review examining the role of both cardiac and vascular alpha(1)-ARs in HF using 5 databases for our search. All three alpha(1)-AR subtypes (alpha(1A), alpha(1B) and alpha(1D)) 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 alpha(1)-ARs. Conflicting findings arise from different studies concerning the influence that HF has on alpha(1)-AR expression and function; in contrast to beta-ARs there is no consistent evidence for down-regulation or desensitization of cardiac or vascular alpha(1)-ARs. Whether alpha(1)-ARs are a therapeutic target in HF remains a matter of debate.