What is the clinical effect of vagal stimulation by muscarinic receptors?
bradycardia
Cholinergic stimulation of muscarinic receptors in endothelial cells releases ___________ which produces ____________
nitric oxide
vasodilation
How do cholinergic drugs treat glaucoma?
they constrict ciliary muscle and open the canal of schlemm reducing internal pressure in the eye ball
What happens when postganglionic parasympathetic nerves that innervate glandular cells in the digestive and respiratory systems are stimulated?
cells secrete
Lacrimation, or watery eyes, is caused by __________ action on lacrimal glands
cholinergic
What can block the cholinergic affect in sweat glands causing the muscarinic receptors to secrete?
atropine
__________ _________ are used to improve bladder function and reduce urinary retention
muscarinic agonists
Acetylcholine binds with ___________ receptors at the myoneural junction in skeletal muscles of the somatic nervous system
nicotinic
Where is acetylchline synthesized?
the cytoplasm of the nerve terminals
What is acetylcholine synthesized from?
acetyl coenzyme A (CoA) and choline - put then together....
ACETYLCHOLINE
Where are acetyl coenzyme A and choline stored before they make acetylcholine?
vesicles located within cholinergic neurons at the prejunctional and postjunctional nerve endings (including pre and postganglionic nerves of the PNS, and preganglionic nerves in the SNS)
true or false. When the nerve impulse stimulates the release of Ach at the nerve ending, the neurotransmitter crosses the junction and reversibly binds to Ach receptors on the postganglionic fibers
true
What happens after the effect of Ach binding to the receptor on the postganglionic fiber takes place?
Ach is released from the binding site and is degraded by acetylcholinestrase
What is the enzyme that degrades acetylcholine?
adetylcholinesterase (found in junctional fluids)
It separates the choline component from the acetate fraction
What happens to the choline after acetylcholine is degraded? And to the acetate?
choline is absorbed by the nerve to form more Ach
acetate enters the metabolic pool
Is destruction of Ach fast or slow? how does this affect the duration of receptor activation?
destruction is rapid
duration of receptor activation is short
The SNS functions to provide for ________ of body function monitorying and readjusting organ systems.
homeostasis
The SNS is said to function as a _____ a feature used during the stress response
unit
What is the prototype adrenergic stimulant?
epinephrine
Why is epinephrine used in dentistry?
because of its vasoconstrictive properties; which reduces systemic toxicity and prolongs the duration of the anesthetic action, and reduces intraoperative bleeding
true or false. Epinepherine and Ach cdan activate different receptor sites.
true
What are the different receptor sites that epinepherine can activate?
alpha and beta
Why does epinepherine have a significant cardiovascular effect?
because beta-1 receptors predominate in the organ
What is a positive inotropic effect?
increase of the force of the cardiac muscle contraction (epinepherine can have this effect)
What is a positive chronotropic effect?
stimulation of the sino-atrial (SA) node pacemaker cells to increase the heart rate (epinepherine can have this effect)
increase cardiac output
increased amount of blood pumped out of the heart (epinepherine can have this effect)
Why does increasing the heart rate have a negative effect?
because it decreases atrial filling because there is less time between beats to accommodate for atrial filling
Another negative effect of epinepherine on the cardiovascular system is that it increases the cardiac workload causing an increased need for oxygenated blood; What can the decrease in cardiac efficiency result in?
muscular hypoxia
true or false. ventricullar arrhythmia and fibrillation can result when high doses of epinepherine are administered systemically
true
What happens in the adrenal medulla to stimulate the release of epinepherine and norepinepherine?
acetylcholine binds with nicotinic receptors
The adrenal medulla is part of the SNS but acts as its own _____________
postganglionic fiber
What type of receptors predominate in the blood vessels in the body, exept for blood vessels in skeletal muscle?
alpha-1 receptors
What type of receptors predominate in the skeletal muscle?
both alpha-1 and beta-2
The _________ of epinepherine can affect which receptors are activated and influence sympathetic effects
concentration
In the skeletal muscle vascular bed, ________ receptors have a greater affinity to epinepherine than do ______ receptors
beta-2
alpha-
In the skeletal muscle vascular bed, small doses of epinepherine causes vaso-___________ and _________ blood flow; large doses of epinepherine causes vaso-__________ and ________ blood flow, but as the tissue level of EPI falls, vaso-__________ again prevails
dilation
increased
constriction
decreases
dilation
How does the adrenergic vasoconstrictor isoproterenol affect the lungs and blood vessels; and how does it affect the cardiac muscles?
it binds to beta-2 receptors causing vasodilation and bronchodilation
it acts on beta-1 receptors and stimulates cardiac muscle
How does stimulation of the adrenergic nerves in vascular beds of salivary glands affect them?
binds to alpha receptors and causes vasoconstriction, it also inhibits secretions (xerostomia)
Why does epinepherine cause increased blood pressure?
because alpha receptors predominate in the peripheral blood vessels, the high blood pressure is caused by vasoconstriction
In coronary arteries, vasoconstriction usually dominates, but the effect may be obscured, how so?
by local vasodilation as a result of relative hypoxia that may occur when EPI causes increased myocardial contraction
What is the net effect of EPI on the cardiovascular system as a whole?
beta-mediated vasodilation and alpha-mediated vasoconstriction; with vasodilation predominating at low doses
What is the most significant effect of epinepherine on the respiratory system?
beta-2 receptors in the smooth muscle of the bronchioles; beta adrenergic agonists can revers bronchoconstriction associated with asthma or anaphylaxis
How does epinepherines interaction with alpha-1 receptors in vascular smooth muscle of bronchiloar mucosa help to relieve mucosal congestion?
they cause vasoconstriction there and increase the blood flow to help brochioles dilate
What do adrenergic agonists do to the smooth muscle of the wall of the stomach and intestines? What receptors mediate this effect?
inhibit it, decreasing both tone and motility resulting in constipation
both alpha and beta receptors (this is an exception to the rule for the alpha receptor effects)
What does alpha-1 receptor activation do to the eye? What does beta-2 receptor activation do to the eye?
contraction of the radial muscle of iris (pupil dilation)
relaxes ciliary muscle which increases ligament tension on lens and decreases the angle of lens curvature
How does epinepherine affect the bladder?
produces the retention of urine by beta receptors causing relaxation of the detrusor smooth muscle walls; and alpha receptors cuasing constriction of the trigone and sphincter
When triglyceride is broken down, effect that is influenced by epinepherine, resulting in the release of free fatty acids and glyecerol in to the circulation, what does this do for the body?
increases energy sources
What chemical is the official neurotransmitter of the SNS at the effector organ?
norepinepherine
What chemicals belong to the class known as catecholamines?
norepinepherine and epinepherine
Where is norephinepherine made and stored?
made by cells in the reserve pool
stored in the mobile pool
When and where is norepinepherine released?
it is released through the nerve action potential at the junction of the postganglionic fiber and the effector organ
Norepinepherine binds to a receptor once it is released, what happens when it is released from the receptor?
it is reuptaken into the adrenergic nerve terminal and stored, ready to be released again for receptor activation.
Does norepinepherine have to be resynthesized like acetylcholine? What affect does this have on the duration of the adrenergic affect?
