In skeletal muscle :
Epinephrine causes glycogen breakdown. In response to stress, there is a need to mobilize glucose- release it from storage so it can be broken down to provide energy. Therefore need to increase glycogen breakdown (and decrease glycogen synthesis) in muscle (and liver). PKA is activated in skeletal muscles, which phosphorylates phosphorylase kinase, glycogen phosphorylase, thus decreasing its activity of glycogen synthesis.
In smooth muscle of lung:
Epinephrine causes muscle relaxation. in response to stress, need to breathe more deeply. Therefore, smooth muscles around the tubes that carry air, (bronchioles) relax. In smooth muscle surrounding the bronchioles, PKA phosphorylates a protein (MLCK), which is an active kinase needed for muscle contraction. MLCK must bind Ca2+ (in the form of a calmodulin/ Ca2+ complex). If MLCK is phosphorylated, the Ca2+/calmodulin complex cannot bind to it, and contraction does not occur.
However, in peripheral circulation, smooth muscles around blood vessels (arterioles) contract, diverting blood from peripheral circulation to essential internal organs.
There are two basic types of epinephrine receptors- called alpha and beta adrenergic receptors. these two types of receptors activate different G proteins and generate different second messengers.
a) beta-receptors- G protein type(Gs)- cAMP response- PKA- relaxation
b) alpha-receptors- different G protein (Gp)- IP3 (second messenger)- binds to receptor on ER membrane-m opens Ca2+ channels in ER- Ca2+ release- contraction.
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