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39 Cards in this Set

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  • Back
Where is the a-2 AR located? What action occurs when it is bound?
*the pre-synaptic membrane
*inhibits further release of NE
Rank the affinity of NE, epi, and isoproterenol to the alpha ARs?
epi > NE >>> iso (no effect)
What is the effect of binding the a-1 AR?
Causes vasoconstriction in vascular smooth muscle.
Rank the affinty of epi, NE, and isoproterenol on the B-1 and B-2 ARs.
B-1: iso > epi = NE

B-2: iso > epi >>> NE (no effect)
In what kind of tissue are B-2 ARs usually found?
Tissue that is not inervated by sympathetic neurons.
What effect does activation of B-1 ARs in the heart have?
Increases HR and CTY.
What effect does binding B-2 ARs in smooth muscle have? Those in the liver?
*Smooth muscle: relaxtion of vascular and bronchial smooth muscle

*liver: glycogenolysis
How many types of ARs are there?
Nine:
3 x B subtypes
3 x a-1 subtypes
3 x a-2 subtypes
What effect does isoproterenol have on the heart?
Binds B-1 receptors to cause an increase in HR and CTY, and thus CO.
What effec does NE have on bronchial smooth muscle?
Very little - it binds poorly to B-2 ARs here.
How is the effect of binding a B AR modulated - i.e. what are the downstream effects?
The B ARs are G-protein linked and cause an increase in intracellular cAMP.
How do caffeine and theophylline mimic B AR stimulation?
They inhibit a phosphodiesterase thus increasing the intracellular cAMP.
What is desensitization? What is the usual molecular mechanism?
After prolonged stimulation the receptor changes to a form that does not produce the same response when stimulated. This is usually due to phosphorylation of the receptor.
How does maintenance therapy of asthma with B-2 agonists create a danger for acute attacks?
Prolonged stimulation results in desensitization of the B-2 receptors which are then less responsive to agents used to treat acute attacks.
Describe how B-1 blockers used to treat HTN can precipitate a withdrawal syndrome if suddenly discontinued.
Antagonism of the B-2 blockers results of upregulation of the receptors and of the downstream signalling molecules. When the drug is removed endogenous NE binds these "supersensitive" receptors and causes a large sympathetic innervation.
Describe the adrenergic innervation of the heart. What are some negative effects?
B-1 ARs are activated by iso, NE, and epi. This produces an increase in intracellular calcium which raises HR, CTY, and CO.

Angina and arrhythmias are possible.
What effect does adrenergic stimulation have on the efficiency of the heart?
It increases CO and greatly increases oxygen consumption, thus efficiency (CO/O2) is decreased.
What adrenergic receptors are found in vascular smooth muscle? What are the effects of activation?
a-1 ARs cause contraction and vasoconstriction when bound.

B-2 ARs cause relaxation and vasodilation when bound.
What are the effects of epi and NE on the ARs in vascular smooth muscle?
Epi binds a-1 and B-2 and thus can cause constriction or dilation depending on the tissue.

NE binds a-1 and causes constriction. It does not bind B-2 with great affinity.
Describe the adrenergic innervation of the vessels of the skin and mucosa.
a-1 ARs dominate, thus adrenergic innervation causes vasoconstriction.
Describe the adrenergic innervation of the vessels of the kidneys and abdominal organs.
a-1 ARs dominate, thus vasoconstriction occurs.
Describe the adrenergic innervation of the vessels of the liver and skeletal muscle.
B-2 ARs dominate, thus vasodilation occurs.
Describe the adrenergic innervation of the capacitance veins.
a-1 ARs dominate, thus vasoconstriction occurs to increase venous return to the heart.
How does epi affect bronchial smooth muscle?
It binds B-2 ARs to cause relaxation and dilation of the bronchial passages.
How do NE and epi affect the spleen? Which has the stronger effect?
a-1 ARs are bind and cause contraction of the smooth muscle capsule of the spleen. This increases the number of blood cells in circulation.

Epi binds a-1 ARs with greater affinity, thus it has the stronger effect.
How does adrenergic stimulation affect the uterus? Which plays the bigger role: epi or NE?
Epi binds B-2 ARs to cause relaxation of the smooth muscle. NE does not bind with very high affinity.
What effect does sympathetic innervation have on the seminal tract?
a-1 ARs are activated and cause contraction of smooth muscle and constriction of the tract.
What effect does sympathetic innervation have on the pupil?
Activation of a-1 ARs in the ciliary radial muscles cause mydriasis (pupillary dilation).
How can glaucoma be treated by B-1 antagonists?
Blocking B-1 ARs in the ciliary epithelium inhibits the production of aqueous humor.
How can glaucoma be treated with a-2 agonists?
Binding a-2 agonists prevents further release of NE, thus decreasing B-1 activated production of aqueous humor by the ciliary epithelium.
How can glaucoma be treated with B-2 agonists?
Stimulation of B-2 ARs in the ciliary muscle will cause relaxation and increase outflow of aqueous humor.
How is the hypertensive effect of NE release accentuated by the kidney?
NE binds JG cells in the kidneys and stimulates release of renin which raises BP.
What kind of AR are found in the pili erector muscles?
a-1 ARs which causes conttraction when stimulated.
Describe the sympathetic innervation of sweat glands.
99% are innervated by postganglionic sympathetic neurons which release ACh.

1% are innervated by postganglionic sympathetic neurons which release NE that binds a-1 ARs.
How does adrenergic stimulation reduce sympathetic outflow at the level of the medulla? What are two drugs that induce a hypotensive effect by action at at this level?
NE binds a-2 ARs which inhibits further release of NE and decreases sympathetic outflow.

Clonidine and aldomet are a-2 agonists selective to these receptors.
What are the net cardiovascular effects of isoproterenol?
Activates B-1 ARs in the heart and B-2 ARs in the vascular smooth muscle. The net effects are:
*increased heart rate
*increased CTY
*increased systolic BP
*decreased diastolic BP
*increased pulse pressure
What are the net cardiovascular effects of NE?
Binds B-1 ARs in the heart to directly increase HR and CTY. Binds a-1 ARs in the vascular smooth muscle to cause vasoconstriction. Increased BP triggers the baroreceptor reflex and an indirect decrease in the heart rate through vagal stimulation is seen. Net effects are increased BP and decreased HR.
What are the net cardiovascular effects of NE in a patient pre-treated with atropine?
Atropine is a muscarinic blocker which inhibits vagal transmission in the heart. Net effects are increased BP and HR.
What net cardiovascular effects are seen with NE given to a patient treated with an a-1 antagonist?
This blocks the vasoconstrictive effect thus only increased heart rate is seen.