Is the adenosine A(2B) 'biased' receptor a valuable target for the treatment of pulmonary arterial hypertension?

Pulmonary arterial hypertension (PAH) is a maladaptive disorder characterized by increased pulmonary vascular resistance leading to right ventricular failure and death. Adenosine released by injured tissues, such as the lung and heart, influences tissue remodeling through the activation of adenosine receptors. Evidence regarding activation of the low-affinity A(2B)AR by adenosine points towards pivotal roles of this receptor in processes associated with both acute and chronic lung diseases. Conflicting results exist concerning the beneficial or detrimental roles of the A(2B) 'biased' receptor in right ventricular failure secondary to PAH. In this review, we discuss the pros and cons of manipulating A(2B)ARs as a putative therapeutic target in PAH.