How would you expect a non-hydrolyzable GTP analogue to affect signalling events that take place following exposure of a cell expressing α2-adrenergic receptors to:
4) All of the above in the prescence of pertussis toxin or cholera toxin?
Good question, I will try to be careful in my answer.
I will assume that by "expressing α2 receptors" you mean that these are smooth muscle cells (SMC) and because you are asking about β-agonists I will assume the presence of β-adrenergic receptors. For clarification we will assume that these receptors are equally proportional in their density within the plasma membrane.
That said it will be of importance to note that α2 receptors result in constriction and β receptors result in relaxation of the SMC. Both α2 and β are G-protein receptors with 7 transmembrane domains and three subunits ...