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Flashcards in ANS lecture 2 week 3 Deck (26):

True or false: Somatic and autonominc nervous systems are controlled simutaneously from interacting components of one brain and one spinal cord-there are not two nervous systems. For example, the hypothalamus is the highest brain center that direectly regulates the ANS but it also regulates many fxns that are not part of the ANS. All stimuli that affect the somatic system also directly or indirectly affect the ANS.



How does the ANS have effects on behavior?

The ANS, through visceral rxns, molds and determines the quality and nature of behavioral rxns. Visceral rxns are based largely on previous experience and conditioning. Conditioning and learning are emotional and nostalgic components as well as autonomic rxns that are retained in memory that can be kept longer and called upon more readily than the recall of specific events or the repeating of mechanical, somatic actions. 


What are the effects of sympathetic and parasympathetic innervation to the heart? What are the differences in innervation of the heart as it pertains to the right and left vagus nerve?

S: Produces an increase in both heart rate and myocardial contractility

PS: Causes cardiac decelertion. The right vagus nerve primarily innervates the SA node and the left vagus nerve primarily innervates the AV node. 


What are the effects of sympathetic and parasympathetic innervation to arterioles? Discuss the differences in sympathetic innervation to arterioles as it pertains to skeletal muscle.

S: The responses of an organ in reaction to autonomic stimulation can be complex, and not easily summarized by single words within a table. A notable example is the response of arterioles of skeletal muscle to sympathetic stimulation. There is both adrenergic and cholinergic sympathetic innervation. The cholinergic nerves are not tonically active; they are activated as an anticipatory part of fight or flight. Cholinergic activation leads to vasodilation. But this response is short lived. It is probably the main mechanism for vasodilating shunt vessels (which do not directly supply skeletal muscle). This allows a rapid increase in cardiac output without significant increases in arterial pressure, 
conducive for exercise. There is a subsequent direct adrenergic response, which causes vasoconstriction. But with sustained use of the muscle, metabolic products build up which cause vasodilation (and which override 
sympathetic influences). This is the response listed in Table 1. For arterioles throughout the systemic circulation, vasconstriction is generally the dominant sympathetic response.

PS: Blood vesseles are not generally innervated by the parasympathetic NS, however, engorgement of sexual erectile tissue is mediated by parasympathetic vasodilation. 


What are the effects of sympathetic and parasympathetic innervation to veins?

S: Bc 70 % of the blood is in veins, regulation of venous capacity is an important determinant of distribution of systemic blood volume. As an essential regulator of venous return to the heart, venous capacity is also an important regulator of CO. Much of the venous system is lined by smooth muscle and through smooth muscle contraction, sympathetic stimulation induces vasoconstriction-decreases radius-increases resistance-increases pressure gradient-increased return

PS: does not innervate veins


What are the effects of sympathetic and parasympathetic innervation to bronchi? Which system is more important for controling bronchodilation and constriction?

S: Although there is some, sparse innervation of bronchi which cause them to dilate, it is generally thought that most of the sympathetic dilation is due to circulating epinephrine. 
PS: Its post-ganglionic innervation, denser than that of the sympathetic nervous system, causes constriction of the bronchioles. 


What are the effects of sympathetic and parasympathetic innervation to abdominal viscera? How are the proximal and distal portions of the colon innervated differently as it pertains to the parasympathetic NS?

S: Sympathetic stimulation inhibits secretion of digestive juices, reduces the strength of peristalsis, and promotes vasoconstriction.
PS: Stimulation produces secretion of digestive juices, and increases motility of the stomach, intestine, and colon. The vagus innervates the proximal portion of the colon, whereas sacral segments of the spinal cord innervate the distal portion of the colon.


What are the effects of sympathetic and parasympathetic innervation to pelvic viscera (lower bowel and urinary bladder)? Use the bladder as an example to state what parts are innervated the two branches of the ANS, what receptors each uses, the NTs, and what the effects are. What is the most important factor for controlling the pelvic cavity?

Like abdominal viscera, increased sympathetic output inhibits activity whereas increased paraysmpathetic output is stimulatory. However, voluntary, conscious decisions are more important for pelvic than for abdominal activity. The bladder stores urine that is elminated through an outlet that consists of the neck of the bladder, the urethra, and striated muscles of the spinchter of the urethra. Parasympethetic nuerons originating in the sacral cord send excitatory neurons to the smooth muscle walls of the bladder causing their constricition. Parasympathetic innervation also causes relaxation of the urethral smooth muscle through NO. These actions promote bladder emptying. 

The sympathetic NS promotes relaxation of smooth muscle in the bladder through acting on B2 adrenergic receptors and contraction of the urethra thorough stimulation of alpha1 adrenergic receptors. Conscious somatic control is exerted through motorneurons that innervate the spinchter striated muscles. 


What are the effects of sympathetic and parasympathetic innervation to the eye? Which branch plays a larger role in regulating pupil size?

S: Stimulation causes dilation of the pupil, but pupil size is primarily controlled by parasympathetic innervation of the sphincter muscle. 
PS: Accommodation of the lens is produced by contraction of the ciliary muscle. Parasympathetic activation causes the ciliary muscle to contract, producing pupil constriction.


What are the effects of sympathetic and parasympathetic innervation to the skin? What NT is secreted? What bodily fxn is controlled through ANS innervation to skin?

The sympathetic reflexes that promote sweating, called sudomotor reflexes, are very important in temperature regulation. The sweat glands are controlled by sympathetic, but not the parasympathetic, fibers. Despite the fact that the innervation is sympathetic, the post-ganglionic fibers secrete ACh. 


What are the effects of sympathetic and parasympathetic innervation to the salivary glands?

S: Stimulation produces a small amount of viscous saliva, rich in solids. The vasoconstriction that occurs in sympathetic stimulation reduces blood flow to the glands.
PS. Stimulation leads to a copious and watery salivation.


What are the effects of sympathetic and parasympathetic innervation to lacrimal glands? What are lacrimal glands? Which branch of the ANS is more important for secretion from lacrimal glands?

The fluid of tears provides lubrication for the eyelids and helps wash away noxious agents. 
S: Activation constricts blood vessels that supply the lacrimal glands, reducing secretion of tear fluid. 
PS: Promotes secretion. The PS component is of more consequence than the sympathetic component.


What are the effects of sympathetic and parasympathetic innervation to the kidney? What processes of the kidney are controlled through this innervation?

Relative to its size, the kidney is more richly innervated by postganglionic fibers than almost all organs. The innervation is exclusively sympathetic, supplying arterioles, intrarenal arteries, and a multitude of the cells (e.g., smooth muscle and nephrons). Through its vasoconstrictor effects, it regulates glomerular filtration rate, renin secretion from juxtaglomerular cells, and tubular reabsorption (These processes will be presented in the 
Renal Lectures).


What are the effects of sympathetic and parasympathetic innervation to the liver?

Activation of the sympathetic nervous system causes the liver to make glucose available, both through breakdown of glycogen into glucose (glycogenolysis) and more direct synthesis of glucose (gluconeogenesis).


see slide 18 of notes for large table with all effects of S and PS on the various organs.


The transmitters of the ANS exert their effects on target organs via ____ ____.

membrane receptors


What is the difference btwn the receptors in the targets of postganglionic receptors (organs) vs the receptor present on post-ganglionic nerves?

The receptors on effect cells are members of the same gene family (G-protein coupled receptors), have the same folding pattern within membranes (7 transmembrane domains) and a high degree of sequence identity. In contrast, the nicotinic ACh receptor present on the post-ganglionic nerves are not apart of the GPCR family.


The SNS exerts its effects through the release of NE and E onto membrane receptors known as adrenergic receptors. Adrenergic receptors are found in tissues such as the heart, smooth muscle, GI, liver, and brain. How are the classes of adrenergic receptors divided? What are the general effects of stimulating the receptors in each class?

Adrenergic receptors are divided into α and ß receptors. Generally, activtion of α receptors causes smooth muscle contracition and ß adrenergic stimulation produces relaxation. An exception to this rule is in the gut where NE stimulation of either receptor causes relaxation. These receptors are in turn divided into α1, α2, and ß1, ß2, ß3. All of these receptors are GPCRs. Muscarinic receptors of the parasympathetic NS are also GPCRs. Each of these subtypes have their own mechanism of action. While activation of the same subtype of receptor will produce the same second messengers in all tissues, the consequences of receptor activation will vary with cell and tissue. 


What is the difference in affinity for NE and E of B1 and B2 adrenergic receptors?

What does activation of B receptors result in intracellularly?

What is the effect of B-adrenergic stimulation in skeletal muscle and liver cells?

What is the effect of B1 receptor stimualtion in the heart? What is the effect of B receptor stimulation in vascular smooth muscle?

Epinephrine is only somewhat more potent than NE at B1 receptors, whereas epinephrine is much more potent (roughly 10-50x) more potent at B2 receptors. 

Activation of B receptors stimulates adenylyl cyclase (AC) through a stimulatory G protein (αs). AC turns ATP into cAMP. Which binds to and activates PKA. PKA has 2 regulatory and 2 catalytic subunits. When intracellular cAMP is elevated, it binds to the regulatory subunits of PKA, the PKA complex dissociates into an R2 dimer and two free catalytic subunits (see slide 24 of notes). The free catalytic subuints of PKA are active and phosphorylate target proteins. 

In skeletal muscle and liver cells, B-adrenergic stimulation leads to the breakdown of glycogen.

You should know the effects of B1 receptor stimulation in the heart. In smooth muscle, activation of B receptors increases cAMP levels which increases PKA. PKA phosphorylates myosin-light-chain kinase MLCK, therefore inhibiting it. MLCK phosphoryaltes and activates myosin for smooth muscle contraction. The phosphorylation and inactivation of MLCK therefore causes relaxtion of vascular smooth muscle-vasodilation.


B adrenergic receptors are present in all vascular smooth muscle.

False. B adrenergic receptors are NOT present in all vascular smooth muscle. 


What are G-proteins? What are their subunits and what effects do their subunits have? What effect does the cholera toxin have on G-proteins that causes diarrhea?

Adrenergic receptors couple to their effectors through G-proteins. G proteins are heterotrimeric: composed of alpha, beta, and gamma subunits. The alpha subunits are diverse (16 genes, 20 diff gene products). The type of alpha subunits largely determines the effector to which the G-protein coupels and whether the effector is stimulated or inhibited. For examaple, αs stimulates AC. Howver, in some cases, the beta and gamma subunits are more important than the alpha subunit in controlling the effector protein. There are 5 beta subytpes that share 50-90% sequence identity and there are 12 gamma subunits. Not all combinations of beta and gamma subunits occur. The beta and gamma subunits are inseparable and can transmit info independly of the alpha subunit. When activated by a receptor that has a bound agonist, GDP-GTP exchange takes place on the alpha subunit and it dissociates from the beta and gamma subunits (then get active alpha subunit and a beta-gamma complex).

The cholera toxin binds to the alpha subunit of a G-protein in the gut and when bound, the alpha subunit is unable to associate from AC. cAMP levels become patholgoically elevated. In the intestine, cAMP promotes Cl- and Na+ efflux. Water movement into the intestinal lumoen osmotically follows and causes massive diarrhea. 


What is the difference in affinity of NE and E at alpha 1 and alpha 2 adrenergic receptors?

NE is considerably more potent at both alpha 1 and alpha 2 receptors than E.


What are the intracellular results of stimulating   α2 adrenergic receptors? Give an example in the body.

What effect do alpha 2 adrenergic receptors have in the presynaptic terminals of postganglionic sympathetic fibers? What is this process called?

 Stimulation of alpha 2 receptors is similar to that of B receptors with an important difference-alpha 2 receptors are coupled to AC via an inhibitory alpha subunit (αi) of Gi. This results in a decrease in cAMP levels. In vascular smooth muscle, stimulation of these receptors opposes that of B receptors. alpha 2 adrenergic stimulation leads to decreased levels of activated PKA which leads to incresed levels of activated MLCK--->contraction of smooth muscle---> vasoconstriction.

There are presynaptic alpha 2 adrenergic receptors on postganglionic sympathetic fibers. Therefore, release of NE leads to inhibition of presynaptic AC which in turn causes dephosphorylation of Ca2+ channels in the presynaptic terminal. Bc dephosphorylation of Ca2+ channels leads to shorter open time durations, there will be a smaller influx of Ca2+ into the presynaptic terminal---> less NE release. NE locally inhibits the release of more NE. This is referred to as an auto-inhibitory feedback mechanism.


What are the intracellular effects of the stimulation of  α1 receptors? Give and example in the body.

Stimulation of  α1 receptors leads to a rise in intracellular Ca2+. Alpha 1 receptors couple to phospholipase C (PLC) via a G-protein with another subunit, known as αq. PLC catalyzes hydrolysis of phosphoinositol 4,5 phosphate (PIP2) resutling in inositol 1,4,5 phosphate (IP3) and diacylglycerol (DAG). IP3 is soluble in cytoplasm. It diffuses to the ER and stimulates the ER to release Ca2+. DAG remains membrane bound and has many actions including activation of PKC which phosphorylates target proteins. Note that hydrolysis of PIP2 leads to the formation of 2 intracellular messengers which activate independent, but possibly paralle, interacting pathways.

Intracellular Ca2+ concentrations are usually below 10^-7 and maximally rise to about 10^-5 when cells are activated. The increased Ca2+ exerts its effects by binding to Ca2+ binding proteins. One example is calmodulin (CaM). Usually CaM is free, but upon binding of Ca, the calmodulin-Ca2+ complex binds to a target enzyme-Ca+2/calmodulin-dependent kinase which iniates a molecular cascade.

Stimulation of alpha 1 adrenergic receptors in vascular smooth muscle promotes a rise in intracellular Ca2+ which causes activation of MLCK, a CaM kinase. Activated MLCK--->phosphorylation of myosin---> smooth muscle contraction---> vasoconstriction



Acetylcholine exerts its effects via membrane bound receptors known as cholinergic receptors. What are the 2 types of cholinergic receptors?

nicotinic and muscarinic


Where are nicotinic receptors found? How do nicotinic receptors exert their effects (what is result of their stimulation)? What is an agonist and antagonist of this receptor?

Nicotonic receptors occur on the post-ganglionic neurons in the synapses of the autonomic ganglia and at the skeletal muscle NMJ. Nicotinic receptors, when bound to ACh, lead to membrane depolarization (cation channels).

Nicotine is an agonist and curare is an antagonist. 


Where are muscarinic receptors found? What is an agonist and antagonist of this receptor?

What are the types of muscarinic receptors? 

How do muscarinic receptors exert their effects (what is result of their stimulation)? 

What muscarinic receptor is in the heart and what does its activation result in?

Muscarinic receptors occur in the organs innervated by the parasympatheitc postganlgionic endings. Muscarine is an agonist and atropine is an antagonist. Muscarinic receptors are divided into 5 different subclasses:

Activation of odd numbered muscarinic receptors (M1, M3, M5) leads to a rise intracellular calcium through the IP3 system. 

Stimulation of even numbered muscarinic receptors (M2, M4) leads to a decrease in cAMP.

M2 is in cardiac muscle and the acute response to activation of this channel is the opening of K+ channels ---> more negative Vm--> harder to depolarize ---> slows HR