Pharmacological and molecular approaches have shown that an atypical β-adrenoceptor (AR), called β(3)-AR, that is distinct from β(1)-ARs and β(2)-ARs, exists in some tissues in heterogeneous populations such as β(3a)-ARs and β(3b)-ARs. β(3)-ARs belong to a superfamily of receptors linked to guanine nucleotide binding proteins (G proteins). The β(3)-AR gene contains two introns whereas the β(1)-AR and β(2)-AR genes are intronless, leading to splice variants. β(3)-ARs can couple to G(i) and G(s) and they are reported to be present in brown adipose tissue, vasculature, the heart, among other tissues. β(3)-ARs cause vasodilation of microvessels in the islets of Langerhans and may participate in the pathogenesis of cardiac failure, during which modification of β(1)-AR and β(2)-AR expression occurs. The development of β(3)-AR agonists has led to the elaboration of promising new drugs, including antiobesity and antidiabetic drugs. This article reviews the various pharmacological actions of β(3)-ARs and their clinical implications for diabetes and cardiovascular diseases.
Keywords: antidiabetic; vascular smooth muscles; β3-adrenoceptors.