Many hormones and neurotransmitters attenuate cyclic AMP (cAMP) accumulation in intact cells by virtue of their ability to inhibit adenylate cyclase activity via the GTP-binding protein denoted as Gi. Nonetheless, a number of physiological findings suggest that attenuation of cAMP production is not sufficient to serve as the only signal for eliciting the diverse physiological effects provoked by these various receptor populations. Additional biochemical and electrophysiological changes are known to occur after occupancy of receptors linked to inhibition of adenylate cyclase, including acceleration of Na+/H+ exchange, activation of K+ conductances, and inhibition of voltage-sensitive Ca2+ channels. This review summarizes the current understanding of how these receptors are coupled to their multiple potential effector mechanisms and offers some speculation about the possible interplay between the biochemical and electrophysiological sequels of receptor occupancy. It is hoped that future studies will establi...

https://faseb.onlinelibrary.wiley.com/doi/pdf/10.1096/fasebj.2.11.2840317

Receptors linked to inhibition of adenylate cyclase: additional signaling mechanisms.

Simultaneous coupling of alpha 2-adrenergic receptors to two G-proteins with opposing effects. Subtype-selective coupling of alpha 2C10, alpha 2C4, and alpha 2C2 adrenergic receptors to Gi and Gs.

C B Wollheim

Papers

Islet cyclic AMP levels are not lowered during alpha 2-adrenergic inhibition of insulin release.