Activation of a beta receptor by epinephrine or norepinephrine results in activation of the cytosolic messenger cAMP which promotes the opening of the Ca channel during the action potential
The activated beta receptor (a transmembrane protein) induces a series of changes to the membrane bound G protein complex (G proteins are classified as stimulatory (Gs) or inhibitory (Gi); in the case of beta receptor activation a Gs is involved).
The activated Gs protein itself activates the transmembrane enzyme system called adenyl cyclase (also called adenylate cyclase).
The triple combination of beta receptor, G protein complex, and adenyl cyclase is termed the beta-adrenergic system.
Activation of adenylate cyclase produces intracellular cAMP from ATP.
Cyclic AMP is the second messenger of the beta-adrenergic system.
Cyclic AMP induces the activation of a number of third intracellular messengers called protein kinases, specifically protein kinase A (PKA).
Protein kinases phosphorylate various important proteins and enzymes.
PKA phosphorylates the Ca channel protein (L type) enhancing Ca entry into the cell during Phase 2 of the action potential. This starts the process of Ca induced Ca release and contraction.
PKA also phosphorylates phospholamban, releasing the inhibition of SERCA, resulting in Ca uptake by the SR and induction/promotion of diastole and relaxation.
Phosphodiesterases within the cytosol are responsible for the degradation of cAMP promoting the “turning off” of beta stimulation.
Beta2 receptors on the vascular smooth muscle wall are activated mainly by epinephrine
As with Beta receptors on the heart, Beta2 vascular receptors result in the release of cytosolic cAMP.
Cyclic AMP inhibits the myosin light chain kinase, a protein that enables actin-myosin interaction, hence Beta 2 stimulation promotes vasodilation.
PKA, activated by cAMP, is responsible for phosphorylating several proteins involved in contraction and relaxation:
Phosphorylates the L type Ca channels causing an increase in Ca flux into the cell during phase 2 of the action potential.
Phosphorylates the ryanodine receptor causing an increase in Ca released from the SR.
Phosphorylates phospholamban releasing its inhibition of the activity of SERCA causing an increase in Ca uptake in the SR.
Phosphorylates Tn-I thereby decreasing the sensitivity of Tn-C for Ca thus enhancing relaxation.
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