Intro to ANS Flashcards
efferent ANS conduct
impulses to heart, smooth muscle and glands
afferent ANS conduct
visceral pain stimuli and afferent components of autonomic reflexes.
Sympathetic preganglionic fibers leave CNS through
the thoracic and lumbar spinal nerves
Parasympathetic leave CNS through
cranial nerves and sacral spinal roots.
effects of stimulation of sympathetic system
increase heart rate, blood pressure, mobilize energy stores, increase blood flow to skeletal muscles and heart while diverting flow from skin and internal organs, dilate the pupils and bronchioles.
sympathetic reaction is triggered by
direct sympathetic activation of effector organs and by epinephrine released by adrenal medulla
functions of parasmpathetic
maintains essential bodily functions like digestiv rpocesses, elimination of waste. balances the sympathetic system. is generally dominant.
-never discharges as a complete system but rather separately
these receive innervation from the sympathetic only
adrenal medulla, kidney, pilomotor muscles, sweat glands. (blood pressure is mainly sympathetic as well.
all preganglionic efferent ANS fivers and somatic motor fivers to skeletal muscle release
ACH which acts on nicotinic receptors.
all parasympathetic post ganglionic fibers release
acetylcholine which acts on muscarinic receptors.
All sympathtic post ganglionic fibers(except sweat glands) release
norepinephrine which act on either alpha or beta receptors.
Sweat gland post ganglioinic fivers release
ACH on muscarinic receptors.
Dopamine is released by
peripheral sympathetic fibers.
Acetylcholine is synthesized
in the cytoplasm from acetyl CoA and choline which is catalyzed by ChAT (choline acetyltransferase)
Acetyl CoA is synthesized in
the mitochondria
choline is transported from
the extracellular fluid into the neuron terminal by sodium dependent carrier (CHT1) (rate limiting step)
ACh is transported from cytoplasm into vesicles by
carreir protein on vesicle membrane called vesicular ACh trasnporter (VAChT)
VAChT is an antiporter that
couples influx of ACh with an efflux of H+
Release of ACh is dependent on
extraceullar calcium and occurs when an on action potential reaches the terminal and triggers sufficient influx of calcium.
AChE splits ACh into
choline and acetate
Lipid linked species of AChE are embedded
within the post-synaptic membrane and located close to cholinergic receptors ensuring quick inactivation of ACh
aChE is also found
in other tissues like red blood cells.
Butyrylcholinesterase(pseudocholinesterase) is found
in blood plasma, liver and other tissues.
Tyrosineis transported across
the BBB into the adrenergic neuron by System L which is a NA+ independent manner
rate limiting step and the way tyrosine gains entry into the neuron
conversion of tyrosine to L-dihydroxypnenylalanine by the enzyme tyrosine hydroxylase.
L-DOPA is converted to dopamine by
L-aminoaced decarboxylase or DOPA decarboxylase
Vesicular monamine transporter(VMAT) translocates
dopamine into synaptic vesicles in exchange for H+.
in addrenergic neurons, intravesicular dopamine Beta hydroxylase converts
dopamine to NE and Ne is stored until release
in adrenal medullary cells
NEreturns to the cytosol where Phenylethanolamine N methyltransferase (PNMT) converts NE to Epi which is then transported to avesicle for storage.
these are released in addition to NE
ATP, Dopamine beta hydroxylase and peptide cotransmitters
NE and Epi are metabolized by
Catechol- O methyltransferase and monoamine oxidase.
COMT
two forms
- soluble cytosolic form
- membrane bound form anchored to RERE-
catalyzes transfer of methyl from S- adenosylmethionine to Oh of catechol.
found in nearly all cells including erythrocytes.
can act on extraneuronal catecholamines
mao
enzyme located on the outer membrne of mitochondria and expressed on most neurons.
oxidatively daminates monoamines o their corresponding aldehydes, these can be converted in turn by aldehyde dehydrogenase to acids or aldehyde reductase to glycols.
MAO-A preferentially deaminates NE and Epi and srotonin
MAO- B- deaminates dopamine more rapidly than serotonin and NE.
In GI tract plays a protective role preventing acces to the general circulation of ingested indirectly acting amines like tyramine and phenylethylamine.
primary mechanism of termination of action of NE that is physiologically released
simple diffusion away from the receptor site and reuptake into the nerve terminal or into perisynaptic glia or smooth muscles.
Reuptake of NE into nerve terminal
happens by Na dependent NE transporter (NET) (Uptake 1
Indirectly acting sympathomimetics like tyramine and amphetamines can be taken up into nerve endings useing
uptake 1 and displace NE from storage vesicles.
Nicotinic receptors
on plasma membranes of postganglionic cells, on plasma membranes of muscels innervated by somatic motor fivers. and on membrane of cells in the CNS
M1 receptors
Gq receptor
found mainly in CNS and autonomic ganglia,
increased cognitive function-CNS
Depolarization- Ganglia
M2 receptors
Gi receptor
found in heart and presynaptic terminals of peripheral and central neurons. They are INHIBITORY by opening K channells and by inhibiting Ca channels.
responsible for vagal inhibition of the heart
inhibition of ACh and NE release at presynaptic nerve terminals
M3 receptors
Gq receptor
located in smooth muscle and secreptory glands, mainly excitatory: mediate secretions (salivary, bronchial and sweat) and contraction of visceral smooth muscle.
can also cause relaxation of VASCULAR smooth muscle via release of NO from endothelial cells. the vasculature has M3 receptors but they don’t have innervation by the parasympathetic system. activation leads to rise in intracellular calcium mediated by an increase in IP3. the calcium activates the nitric oxide synthase leading to formation of NO from arginine, NO diffuses into adjacent smooth muscle cells and binds to and activates guanlyl cyclase which makes cGMP from GTP. cGMP dependent protein kinase phosphrylates proteins leading to relaxation and vasodialtion
NO synthase
found in endothelial cells that line blood vessels
catalyze the formation of NO from arginine
potency series for beta adrenergic receptors
isoproterenol is more potent then Epi which is more potent than NE
Beta 1 receptor
Gs receptor
equal affinity for epi and NE
in the her stimulation leads to positive inotropic and chronotropic responses.
NE stimulates renin secretion by direct action on the juxtaglomerular cells of kidney.
Beta 2 receptor
Gs receptor
higher affininty for Epi than NE
tissues with predominance of Beta 2 (vasculature of skeletal muscle) are very responsive to CIRCULATING Epi released by adrenal medulla.
activates hepatic glycogen phosphyrlase
promotes relaxation of smooth muscle by phosphorylation of myosin light chain kinase to inactive form( bronchial, GI, genitourinary)
in skeletal muscle- increases glycogneoysis and uptake of K
pancrease- increased insulin secretion in beta cells, increased glucagon secretion in alpha cells.
Liver- increased glycogenolysis, increased gluconeogenesis
Beta 3 receptor
Gs receptor
equal affinity for epi and NE
activates TAG lipase to release free fatty acids.
Gs can DIRECTLY enhance
the activation of voltage gated Calcium channels in teh plasma membrane of skeletal and cardiac muscles.
Beta induces effects( all three receptors
actiavtes hepatic glycogen phosphorylase, a rate limiting step in glycogenolysis
Protein kinase A which catalyzes phosphorylation of phosphorylase kinse which activates it and catalyzes inactivation of glycogen synthase. which decreases glycogen synthesis.
alpha receptors potency series
epinephrine is greater than NE and alot greater than isoproterenol.
alpha 1
Gq receptor
found on post synaptic membrane of effector organe.
in most smooth muscle- contraction by activation of calmodulin dependent myosin light chain kinase.( vasoconstriction, genitourinary smooth muscle)
In GI- cause hyperpolarization and relaxation by activation of calcium dependent K channels.
In Liver- causes increased glycogenolysis and increased gluconeogenesis
Alpha 2
Gi receptor
located on presynaptic nerve endings reducing NE release and ACh release
postynaptically on other cells like beta cell of pancrease to reduce insulin release.
with platelets- aggregation
with adipocytes- inhibition of lipolysis
they couple to a variety of effectors.
evoke vasoconstriction by opening voltage gated calcium channels.
D1 and D5 receptors
Gs receptor
found in brain and effector tissues like smooth muscle and renal vascular bed. causes relaxation of renal vascular smooth muscle
D2 receptors
Gi receptor found in brain, effector tissues, smooth muscle, presynaptic nerve terminals.
D3 receptors
Gi receptor found in brain
D4 receptor
Gi receptor found in brain and CV system.
ACh release can be inhibited by
ACh acting on presynapatic M2 autoreceptors. and by NE on presynapatic alpha2 receptors.
other inhibitory receptors
A1, H3 and opioid receptors. even some Beta 2 adrenergic heteroreceptors.
NE release can be inhibited by
Alpha 2 receptors.
heteroreceptors on sympathetic nerve terminals M2, 5-HT, PGE2, Histamine, Enkephalin, and DA receptors.
Enhancement of sympathetic NE release
activation of presynaptic Beta 2 adrenergic receptors and angiotensin 2 receptors.
NE infusion
powerful vasoconstrictor (Alpha 1 effect) it increases Mean arterial pressure. if baroreceptors not in tact it will increase heart rate and contractile forces by beta 1 effect
if baroreceptors intact, there will be negative feedback when MAP is increased which will cause a decrease in sympathetic flow in the heart which will mean an increase in parasympathetic discharge on the pacemaker resulting in bradycardia. which is OPPOsiTE of NE direct action.
eye-alpha 1 receptor
pupillary dilator muscle in the iris
when active it will cause contraction of dilator- mydriasis
eye - M3 receptor
pupillary constrictor, ciliary muscle
will cause constriction of iris- miosis
will cause contraction of ciliary muscle (cyclospasm if marked contraction) so that it can focus at short range.. when it relaxes it will cause long range focus .
- this also causes aqueous humor to flow into canal of schlemm which reduces intraocular pressure.
eye-beta 2 receptor
secretory epithelium of ciliary body
causes secretion of ciliary epithelium that produces aqueous humour.
