Adrenal Medulla: catecholamines Flashcards
what is catecholamine release associated with
cortisol
what catecholamine is mostly in blood
norepinephrine
what catecholamine is mostly in the adrenal medulla
epinephrine
primary action of dopamine
neurotransmitter - very little in plasma
how are catecholamines metabolized
adrenal medulla (recycled), CNS, liver, and kidneys
4 stimuli of catecholamine
fight, flight, fear, reproduction
how is epi released
sympathetic nerve stimulates adrenal medulla via Ach to release epi to act on distant target cells
how is norepi released
sympathetic nerve stimulates Ach at the needed area to release norepi for action on target cells at point of release
how is tyrosine made into L dopa
tyrosine hydroxylase with copper cofactor (O2, NADH tetrahydropteridine
how is L dopa made into dopamine
L-aromatic AA decarboxylase and pyridoxal phosphate
how is dopamine made into norepi
dopamine beta hydroxylase, O2, NADH or NADPH
how is norepi made into epi
SAM and phenylethanolamine N methyltransferase
what stimulates dopamine formation into norepi
sympathetic activity
what stimulates norepi formation into epi
cortisol
what inhibits tyrosine formation into L dopa
negative sympathetic feedback and small negative feedback from norepi
where is epi made
cytoplasma of chromaffin cells
how is catecholamine release acutely regulated
Ach binding to adrenal medulla chromaffin cell triggers Ca cascade which promotes exocytosis of epinephrine from secretory granules
how is catecholamine release chronically regulated
stress triggers hypothalamus to release ACTH which releases cortisol. cortisol induces PNMT (enzyme) and SAM to convert norepi to epi. epi is packaged in neurosecretory granules and released
what adrenergic receptor dilates pupil
alpha
adrenergic receptor activates salivary glands
beta 1
adrenergic receptor increases HR and contractility
beta 1
adrenergic receptor dilates airways
beta2
adrenergic receptor decreases motility
alpha2
adrenergic receptor decreases motility
alpha 2 and beta 2
adrenergic receptor increases sphincter contraction
alpha 1
adrenergic receptor for ejaculation
alpha
2nd msgr alpha 1 adrenergic
IP3
2nd msg alpha 2 adrenergic
cAMP
how do a1 and a2 receptors differ
if a1 is triggered, increase IP3 to increase Ca in the cell to cause smooth muscle contraction and gland cell secretion (cutaneous and GI vasoconstiction, urethral sphincter contraction)
if a2 is triggered, cAMP reduces and inhibits the cell
inhibitory or excitatory alpha receptros
usually excitatory
inhibitory of excitatory beta receptors
inhibitory
2nd msgr beta receptors
all act through cAMP through different effects and tissues
what if beta1 receptor triggered
cardiac muscle stimulated and increased tissue metabolism
beta2 receptor triggered
relaxation of muscle in respiratory passages and in blood vessels of skeletal muscle
if camp increase, constriction of gut sphincter
if decrease, muscle vessel dilation and detrusor relaxation
beta 3 receptor triggered
release of FA by adipose tissue for metabolic use in other tissues
what degrades catecholamines
monoamine oxidase and other stuff
what is the final metabolic product of catecholamine breakdown?
regardless of degradation pathway, is vanillymandelic acid (VMA)
plasma profile epinephrine
increase glucose, increase FFA, not much change of AA
how is a2 receptor special
only one that inhibits (decrease cAMP and inhibit cell activity)
