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45 Cards in this Set

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What kind of ligand and receptors are used in the heart in the Sympathetic nervous system? What happens to HR?
Norepinepherine binds to B1 (adrenergic) receptors in the heart. It innervates the SA and AV nodes increasing their conduction velocity, the contractility and heart rate.
Give me the molecular biology involved for sympathetic innervation of the heart.
The sympathetic nervous system acts through G(s) coupled receptors. The activation of these G-coupled protein receptors increases [CAMP] eliciting the increase of Na+ through "funny" receptors = faster depolarization.
What kind of ligand and receptors are used in the heart in the Parasympathetic nervous system? What happens to HR?
Ach binds to muscarinic receptors in the heart. Ach is released by the vagus nerve which innervates the SA node. This decreases your heart rate.
Give me the molecular biology involved for parasympathetic innervation of the heart.
The parasympathetic nervous system acts through G(i) couple receptors. Their activation decreases [CAMP] and directly opens K+ channels = slower depolarization.
You are running through the forrest and you see a pack of wolves. What happens to your body?
Your sympathetic nervous system kicks in: dilation of pupils, decrease in gastric motility, increase of your heart rate and an increase in your blood pressure.
After you run away from the wolves, you rest by leaning on a pine tree. What is happening to your body?
With an increase of BP, your baroreceptors signal your cardiovascular control center (PANS) to decrease your heart rate (wants to go back to homeostatis). This is done through the vagus nerve. There is vasodilation of your blood vessels and their is a decrease of contraction of your heart = decreasing your BP.
What happens if you increase your total peripheral resistance (TPR)?
This will increase your BP through alpha-1 resulting in vasoconstriction of your blood vessels. This will decrease your HR = reflex bradycardia.
What happens if you decrease your total peripheral resistance (TPR)?
This will decrease your BP through B2 or Muscarinic stimulation resulting in vasodilation of your blood vessels. The result will increase your HR = reflex tachycardia.
You give Norepi to your patients what happens to their BP and heart rate?
Norepi will increase the BP and decrease the HR of the patient.
What are the binding efficiencies of receptors for Norepi?
Alpha and B1 effects at low concentrations and at higher concentrations, B2.
What happens to the BP and HR when you block Norepi alpha receptors?
There is a small rise of BP and an increase of HR. This unmasks the Beta receptors.
What happens to BP and HR when you block Norepi beta receptors?
There is an increase of BP with a decrease of HR.
If you bind alpha-1 receptors what happens?
The binding of Norepi to alpha-1 receptors constricts blood vessels = reflex bradycardia.
What are the binding efficiencies for Epi?
Beta 1 and B2 effects at low concentrations and at higher concentrations, alpha.
What are the differences between Norepi and Epi in comparison to HR and BP?
Epi shows a biphasic curve. At [low], there is an increase of BP and a decrease of HR. At [higher] there is a decrease of BP and an increase of HR.
You block Epi alpha receptors, what happens to the HR and BP?
There is a decrease in BP and an increase of HR.
If you block Epi beta receptors, what happens to the HR and BP?
There is an increase of BP and a decrease of HR.
Name two enzymes that degrade Ach. Give their locations.
Acetylcholinesterase: found in synapses and erythrocytes.

Butrylcholinesterase/plasma cholinesterase: found in the serum and liver, is a scavenging enzyme for all drugs.
You give Ach to your patient what happens to their BP and HR?
At [low] of Ach, there is a decrease of BP and an small increase of HR. At [higher], there is a large decrease of BP resulting in direct bradycardia then a reflex tachycardia. Later on, there is Ach release from the adrenal medula.
What receptors are in excess in the lungs? What happens if you block these receptors?
Beta receptors are in excess. Sympathetics will act on these receptors, relaxing the bronchioles and decreasing secretions. Blocking these receptors will result in vasoconstriction and an increase of secretions.
What are the major functions of the Sympathetic Nervous system?
Increase CO, increase blood flow to needed organs, decrease of blood flow to non-essential organs, decrease GI and urinary activity, increase of blood glucose
What kind of drugs mimic the Sympathetic Nervous system?
Sympathomimetics
What kind of drugs inhibit the Sympathetic Nervous system?
Sympatholytics
What are the sites of action of sympathomimetics?
Indirect acting: Releasing agents, MAOIs, Reuptake inhibitors, alpha blockers.

Direct acting: Catecholamines, non-catecholamines
What are the affects of sympathomimetics on smooth muscle?
Bronchial smooth muscle (primarily beta receptors) relax

Heart: increase force of contraction, stroke volume and cardiac output increases, an increase of arrhythmias, an increase of oxygen consumption.
Where are B receptors found?
Blood vessels of visceral organs (kidney and skeletal muscles) contain beta receptors. In addition, beta receptors are in excess in the lung.
What do alpha agonists do? Name an alpha agonist drug.
Vasoconstriction, causing a reflex bradycardia. Phenylephrine.
What do B1 agonist do? Name a B1 agonist drug.
Increase force and rate of contraction of the heart. Dobutamine.
What do B2 agonist do? Name B2 agonist drugs.
The major affect of B2 agonist is a decrease of blood pressure and bronchodilatation. Terbutaline and albuterol.
What are the affects of Norepi?
Norepi decreases the pulse rate and increasing the blood pressure. The peripheral resistance therefore is increased. Norepi binds to alpha receptors at [low] and binds to beta receptors at [high].
What are the affects of Epi?
There is an increase of heart rate and a decrease of blood pressure. The peripheral resistance therefore is decreased. Epi binds to beta receptors at [low] and to alpha receptors at [high].
What are the affects of Isoproterenol?
There is a substantial increase of heart rate and a decrease of blood pressure. There is a substantial decrease of peripheral resistance.
Name sympathomimetic drugs and their actions.
Amphetamine: taken up by presynaptic nerve terminals, displacing NE, EPI from storage sites. They mimic NE and EPI.

Pargyline and Tranylcypromine (MAO inhibitors): enhance NE and EPI effects.

Cocaine, Tricyclic antidepressants (reuptake inhibitors): exaggerate adrenergic responses.

Yohimibine (alpha blockers): enhanced sympathetic activity.
Name sympatholytic agents and their actions.
Alpha-blocker (phentolamine), Beta-blocker (propranolol): inhibit ability of neurotransmitter.

Clonidine (alpha 2 agonist): decrease CNS sympathetic outfow.

Reserpine: interfere with the synthesis and release of NE.
What are the side effects of sympatholytic agents?
Increases blood volume and Na+ retention (decreasing glomerular filtration), sedation and depression.
What are the side effects of alpha blockers?
Nasal stuffiness and increase of GI motility and diarrhea. Postural hypotenision (reflex tachycardia)and impaired ejaculation.
What are the side effects of the beta-adrenergic blocker?
Bradycardia, decrease of cardiac output which may lead to CHF, effect sensitivity to insulin and oral hypoglycemics, bonchoconstriction, increase of TAGS, and decrease of CO (cold extremities).
What are the actions of beta blockers?
A decrease of HR, contractility, CO, conduction velocity of the heart, AV conduction, and cardiac work.

In addition, there is a decrease of renin, glycogenolysis activity, and lipolytic activity./
What are the effects of muscarinic agonists (cholinomimetics, parsympathomimetics)?
Bradycardia, vasodilation via muscarinic receptors in the blood vessels leading to an indirect tachycardia, increased secretions of fluids, bronchoconstriction, increase peristaltic activity, and pupillary constriction.
What is dysautonomia? How do you test for this disease?
It is a rare recessively inherited disease that is characterized by small fiber peripheral neuropathy. To test for this you give METHALCHOLINE = their pupil constrict. Since these patients have less fibers, a small amount will elicit an effect.
Name the 3 classes of Cholinesterase inhibitors. Give me drug examples for each.
1) Revesible competitive (very short) (EDROPHONIUM)
2) Carbamate inhibitior (short duration) (NEOSTIGMINE)
3) Phosphonate (irrevesible inhibitor, lifetime of enzyme) (DFP)

Cholineestarase inhibitors bloks all preganglions.
Where are nicotinic receptors are? Where are muscarinic receptors?
Nicotinic receptors are found preganglionic in both sympathetic and parasympathetics. Muscarinic receptors are found post ganglionic.
Name Antimuscarinic (anticholinergic) agents. What are their side effects.
Atropine, Methlatropine, Ipratropium.

You have an increase of HR, reduced sweating, dry mouth, reduced GI and bladder motility, reduced bronchial mucous secretion and dilation of bronchioles, and sedation of CNS.
Name a Ganglionic nicotinic receptor blocking agent.
Trimethaphan: a short acting ganglionic blocking agent infused via IV during surgery.
What are the effect of Ganglionic nicotinic receptor blockers?
Vasodilation, failure of sweat glands, tachycardia, dilated pupils, decreased GI tract tone, urinary retention, and dry mouth.