Unit 2 - Autonomics IV Flashcards
explain synthesis of NE and E in adrenergic varicosity?
tyrosine (into cytoplasm) –> DOPA –> dopamine –> NE (vesicle) –> E (adrenal medulla)
is NE or E a neurotransmitter or a neurohormone?
NE is a neurotransmitter
E is a neurohormone
what is the receptor interaction and effector cell response of NE and E?
second messenger amplification
how do D1 (dopamine) exert its second messenger effect?
stimulatory GPCR increases cAMP (like beta1/2/3)
what is the adrenergic receptor excitation response?
constriction; Ca++ is made available to myofibrils and increases tension
-Ca++ from intracellular stores and/or transport from extracellular
what is the adrenergic receptor inhibition response?
relaxation; Ca++ is made unavailable to myofibrils and reduces tension
-Ca++ is taken into intracellular stores and/or pumped out
what is the adrenergic receptor metabolic response?
activation of AC
- increased liver glycogenolysis
- increase in plasma glucose and FFA
what are the 3 ways specifically NE can “terminate” its action?
- neuronal reuptake (neuron-specific)
- effector cell uptake (non-specific and high capacity); extra-neuronal
- diffusion into capillaries
what is the primary mechanism for terminating ACh? how is this different from NE?
enzymatic hydrolysis
-NE is reuptake
what and where is MAO?
monoamine oxidase on mitochondria surface
-metabolize NE, E, and other exogenous adrenergic drugs
what and where is COMT?
catechol-o-methyltransferase in cytoplasm of many cells, especially liver
-metabolize NE, E, and other exogenous adrenergic drugs
what are the major metabolites of NE/E that are measured in urine/plasma?
normetanephrine, metanephrine, VMA, MHPG
-for diagnostic purposes (increased plasma metanephrine indicates pheochromocytoma)
what does alpha-me-tyrosine do to modify chemical transmission?
decreases synthesis of NE (sympathetic) by decreasing pre-synaptic Ca++ influx
what does amphetamine do to modify chemical transmission?
increases release of NE (sympathetic)
what does isoproterenol do to modify chemical transmission?
combine with receptor to increase NE (sympathetic)
-increases post-synaptic Ca++ influx and second messengers
what does propranolol do to modify chemical transmission?
antagonist to beta-receptor sites to decrease NE (sympathetic)
-decreases post-synaptic Ca++ influx and second messengers
what does cocaine do to modify chemical transmission?
increases termination step such that synapse activity increases
what is the prominent effector organ and response to receptor activation of beta 1?
heart - increased heart rate and force of contraction
kidney - renin secretion
what is the prominent effector organ and response to receptor activation of beta 2?
arterioles (and arteries in skeletal muscle, coronary) - dilation
bronchial muscle - relaxation
pregnant uterus - N/A
several other sites - metabolic effects increase
what is the prominent effector organ and response to receptor activation of beta 3?
adipose tissue (lipocytes) - lipolysis and thermogenesis increase
what is the prominent effector organ and response to receptor activation of alpha 1?
arterioles in skin, mucosa, viscera, and kidney - constriction (resistance vessels)
veins - constriction
uterus and spleen - contraction
what is the prominent effector organ and response to receptor activation of alpha 2?
presynaptic nerve endings - inhibit NE release and ACh release (gut)
postsynaptic in CNS - decreased peripheral sympathetic tone
what is the prominent effector organ and response to receptor activation of D1?
renal, mesenteric, and cerebral arterioles - dilation
what are the agonist/antagonist for a1?
agonist: phenylephrine
antagonist: prazosin
