Abstract

Adenosine is a nucleoside that impacts the cardiovascular system via the activation of its membrane receptors, named A1R, A2AR, A2BR and A3R. Adenosine is released during hypoxia, ischemia, beta-adrenergic stimulation or inflammation and impacts heart rhythm and produces strong vasodilation in the systemic, coronary or pulmonary vascular system. This review summarizes the main role of adenosine on the cardiovascular system in several diseases and conditions. Adenosine release participates directly in the pathophysiology of atrial fibrillation and neurohumoral syncope. Adenosine has a key role in the adaptive response in pulmonary hypertension and heart failure, with the most relevant effects being slowing of heart rhythm, coronary vasodilation and decreasing blood pressure. In other conditions, such as altitude or apnea-induced hypoxia, obstructive sleep apnea, or systemic hypertension, the adenosinergic system activation appears in a context of an adaptive response. Due to its short half-life, adenosine allows very rapid adaptation of the cardiovascular system. Finally, the effects of adenosine on the cardiovascular system are sometimes beneficial and other times harmful. Future research should aim to develop modulating agents of adenosine receptors to slow down or conversely amplify the adenosinergic response according to the occurrence of different pathologic conditions.

Highlights

  • Adenosine is a ubiquitous nucleoside that comes from the dephosphorylation of ATP and AMP

  • A specific pharmacological profile, called the receptor of reserve, was described in some diseases, such as coronary artery disease or syncope [29]. It seems that this type of receptor, which is characterized by maximal biological effects while only a weak proportion of receptors are activated by the ligand [30], is an adaptive response to compensate for low adenosine levels, low receptor expression levels or both [29]

  • In patients suffering from supraventricular tachycardia, adenosine administration led to Atrial fibrillation (AF) or flutter in 12% of cases, and atrial premature complexes occurred in 58% of cases [62]

Read more

Summary

Introduction

Adenosine is a ubiquitous nucleoside that comes from the dephosphorylation of ATP and AMP. It is released during hypoxia, ischemia, inflammation and beta-adrenergic stimulation [1,2,3,4,5]. Adenosine acts on a number of tissues (including the immune and nervous systems) through the activation of four G-coupled membrane receptors, named A1R, A2AR, A2BR and A3R, as a function of their pharmacological properties and primary sequence [6,7,8]. Adenosine strongly impacts the cardiovascular system mainly through the activation of its receptors. The main effects of adenosine on the cardiovascular system involve heart rate, vasomodulation and blood pressure regulation. The goal of this review is to summarize the impact of adenosine and its receptor activation during several cardiovascular diseases and conditions

Source and Mechanism of Action of Adenosine
Adenosine Receptors
Effects of Adenosine on Vessels
Adenosine and Ventricular Myocytes
Adenosine and Atrial Fibrillation
Effects of Exogenous Adenosine
Syncope in Hypoxic Conditions
Obstructive Sleep Apnea Syndrome
Altitude Hypoxia
Myocardial Ischemia Reperfusion Protection
Adenosine and Vascular Injury and Repair
Adenosine and Systemic Hypertension
Adenosine and Pulmonary Hypertension
Adenosine and Heart Failure
Findings
Conclusions and Future Directions
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.