The human muscarinic M 2 receptor is a functionally important membrane-bound protein that is negatively coupled to adenylyl cyclase and is widely expressed in a range of tissues, including cardiac myocytes, prejunctional cholinergic nerve endings, and smooth muscle. In the airways, M 2 receptors are constitutively expressed on airway smooth muscle (ASM) and, in contrast to muscarinic M 3 receptors, continue to be expressed during primary culture (1). Muscarinic M 2 receptors play an important role in the control of ASM cAMP regulation, being responsible for acetylcholine-mediated inhibition of adenyl cyclase activity. This action ameliorates in part the relaxant effect of agents such as isoproterenol in the airways (2).Despite the cloning of the human muscarinic M 2 receptor gene several years ago (3, 4) the elements important for tran-

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