Final answer:
The adenosine receptor that often causes bronchospasm and systemic vasodilation is known as the A2B receptor. It elicits these effects by stimulating bradykinin production. Unlike adenosine receptors, adrenergic receptors can cause contrasting effects such as vasoconstriction and bronchodilation.
Step-by-step explanation:
The adenosine receptor that causes bronchospasm and systemic vasodilation is typically the A2B receptor. Adenosine receptors are a group of G protein-coupled receptors with A1, A2A, A2B, and A3 subtypes. Among these, the A2B receptor is known for mediating increased vascular permeability and vasodilation, and causing constriction of the bronchioles, leading to bronchospasm. These effects are produced through the stimulation of the generation of bradykinin, a peptide that causes these physiological responses. In contrast, the body's response to the activation of the sympathetic nervous system includes the release of substances like epinephrine that increase heart rate and contractility, constrict blood vessels, and act as a bronchodilator.
Different adenosine receptors play varying roles in circulatory and respiratory functions. The nervous innervation by autonomic nervous systems also plays a crucial role, with the sympathetic nervous system promoting bronchodilation and the parasympathetic system inducing bronchoconstriction.
A distinction must be made between adenosine receptors and adrenergic receptors. While adenosine receptors like A2B can induce vasodilation and bronchospasm, adrenergic receptors, including α-adrenergic and β-adrenergic receptors, have different functions such as vasoconstriction via α-adrenergic receptors and vasodilation and bronchodilation via β-adrenergic receptors. The α-1 adrenergic receptor subtype, for instance, causes vasoconstriction and smooth muscle contraction, while β receptors typically mediate smooth muscle relaxation and increase in heart muscle contractility.