Norepinephrine acting on post-synaptic alpha-1 receptors signals through which pathway to cause vasoconstriction?

Norepinephrine acting on post-synaptic alpha-1 receptors signals through which pathway to cause vasoconstriction?

• A. Gi decreasing cAMP
• B. Gq increasing calcium via IP3 and DAG
• C. Gs increasing cAMP
• D. No effect

Answer: (B)

Activation of post-synaptic alpha-1 adrenergic receptors triggers a Gq signaling cascade. Gq activates phospholipase C, which splits PIP2 into IP3 and DAG. IP3 releases calcium from the sarcoplasmic reticulum, raising intracellular Ca2+; Ca2+ binds calmodulin and activates myosin light-chain kinase, driving smooth muscle contraction. DAG activates protein kinase C, reinforcing the contraction signaling. The result is vasoconstriction of vascular smooth muscle, increasing systemic vascular resistance and blood pressure. This pathway is distinct from Gi (which would lower cAMP) and Gs (which would raise cAMP) and therefore correctly explains alpha-1–mediated vasoconstriction.

Activation of post-synaptic alpha-1 adrenergic receptors triggers a Gq signaling cascade. Gq activates phospholipase C, which splits PIP2 into IP3 and DAG. IP3 releases calcium from the sarcoplasmic reticulum, raising intracellular Ca2+; Ca2+ binds calmodulin and activates myosin light-chain kinase, driving smooth muscle contraction. DAG activates protein kinase C, reinforcing the contraction signaling. The result is vasoconstriction of vascular smooth muscle, increasing systemic vascular resistance and blood pressure. This pathway is distinct from Gi (which would lower cAMP) and Gs (which would raise cAMP) and therefore correctly explains alpha-1–mediated vasoconstriction.