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Flashcards in ANS Deck (146):
1

How do muscarinic receptors act

they are G-protein coupled receptors

2

How to nicotinic receptors act

They are ion-channel mediated (increase Na+ movement into cells)

3

Types of nicotinic receptors

NM and NN

4

Effects of M2 receptors

Heart: reduce HR, FOC and CO

5

Effects of M3 receptors

1. blood vessel: vasodilation and and decrease BP 2. smooth muscle: contraction--> broncospasm, diarrhea, urination 3. Pupil: miosis 4. Glands: increase salivation (increase lacrimation), sweating, gastric acid

6

M1 receptor type

Gq

7

Effector enzyme at Gq

Gq-->stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

8

Effector enzyme at M1

Gq-->stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

9

M3 receptor type

Gq

10

Effector enzyme at alpha 1

Gq-->stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

11

Effector enzyme at M3

Gq-->stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

12

alpha 2 receptor type

Gi

13

Gq second messenger

stimulates PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

14

alpha 1 receptor type

Gq

15

beta 1 effector enzyme

Gs-->stimulate adenylyl cyclase-->increase cAMP

16

M2 receptor type

Gi

17

Gi effector enzyme

Gi-->inhibit adenylyl cyclase-->decrease cAMP

18

alpha 2 effector enzyme

Gi-->inhibit adenylyl cyclase-->decrease cAMP

19

Receptors that act via Gs

beta 1, beta 2, beta 3

20

M2 effector enzyme

Gi-->inhibit adenylyl cyclase-->decrease cAMP

21

beta 2 effector enzyme

Gs-->stimulate adenylyl cyclase-->increase cAMP

22

Receptors that act via Gq

M1, M3 & alpha 1

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beta 1 receptor type

Gs

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beta 2 receptor type

Gs

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beta 3 receptor type

Gs

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M1: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gq 2. Stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3. Neurons 4. CNS effects

27

Receptors that act via Gi

alpha 2, M2

28

Effect of tyrosine hydroxylase

converts Tyrosine-->DOPA RATE LIMITING STEP in formation of Dopamine ADRENERGIC TRANSMISSION

29

NN receptor 1. location 2. type

1. ANS ganglia & Adrenal Medulla 2. Na/K channel

30

alpha 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gi 2. Inhibit adenylyl cyclase-->decrease cAMP 3. presynaptic neurons 4. reduces release of norepinephrine-->bradycardia & hypotension

31

M3: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gq 2. Stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. Smooth muscle and; glands: -->contraction (except in bv-->vasodilation-->decrease BP); diarrhea, bronchoconstriction, urination, increase secretions, salivation, stomach acid, sweating, lacrimation Pupil and ciliary muscle: contracts-->miosis; increase flow of aqueous humor

32

alpha 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gq 2. Stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. blood vessels--> vasoconstriction-->increase BP pupil (iris)-->dilation (mydriasis) smooth muscle-->sphincter contraction-->constipation & urinary retention

33

Metyrosine

inhibits tyrosine hydroxylase-->so it can't convert tyrosine to DOPA AFFECTS ADRENERGIC TRANSMISSION Tyrosine is co-transorted into pre-synaptic nerve terminal with Na+

34

beta 3 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gs 2. stimulate adenylyl cyclase-->increase cAMP 3. fat tissue 4. Lipolysis

35

Rate-limiting step for ACh synthesis

choline uptake

36

M2: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gi 2. Inhibit adenylyl cyclase-->decrease cAMP 3. Heart 4. reduces HR, FOC and CO

37

Receptor in adrenal medulla & response

NN-->secretion of Epi & NE

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beta 3 effector enzyme

Gs-->stimulate adenylyl cyclase-->increase cAMP

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Where you find NN

Adrenal medulla & autonomic ganglia

40

beta 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gs 2. stimulate adenylyl cyclase-->increase cAMP 3/4. smooth muscles--> relaxation-->bronchodilation, urinary retention, constipation, uterus relaxation liver--> heart-->

41

beta 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

1. Gs 2. stimulate adenylyl cyclase-->increase cAMP 3. heart 4. contraction, increased HR increases renin release & juxtaglomeruluar apparatus

42

Reserpine

inhibits uptake of dopamine into vesicles (inhibits storage) AFFECTS ADRENERGIC TRANSMISSION

43

Bretylium

inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release-->inhibits release AFFECTS ADRENERGIC TRANSMISSION

44

Guanethidine

inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release-->inhibits release AFFECTS ADRENERGIC TRANSMISSION

45

cocaine

inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION

46

Tricyclic antidepressants

inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION

47

Where does NE work

at presynaptic alpha 2 (autoreceptors) & at postsynaptic alpha 1 receptors

48

Hemicholinium

AFFECTS CHOLINERGIC TRANSMISSION inhibits uptake of Choline into presynaptic nerve terminal (co-transorter with Na+); RATE-LIMITING STEP

49

Vesamicol

AFFECTS CHOLINERGIC TRANSMISSION inhibits storage of ACh in the presynaptic nerve terminal (ACh can't be properly taken up & stored in vesicles)

50

Botulinum

AFFECTS CHOLINERGIC TRANSMISSION inhibits release of ACh (vesicles can't properly dock & release)

51

rate limiting step for catecholamine synthesis

tyrosine hydroxylase

52

Cholinergic neurotransmission is terminated by

AChE

53

Adrenergic neurotransmission is terminated by

reuptake

54

DAG function

modulates action of protein kinase C

55

Myasthenia Gravis Symptoms; Dx; what makes it worse?

autoimmune disorder that involves antibody mediated disruption of NMJ receptors Production of antibodies that decreases the number of functional nicotinic receptors on the muscle end plates Sx: transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness. Severe disease may affect all muscles including those used in respiration infection and thyroid dysfunction worsen the symptoms Dx = blood ACh receptor antibody level

56

result of IP3

IP3-->Ca2+ release from intracellular storage-->smooth muscle contraction

57

Somatic nervous system receptors & are they cholinergic or adrenergic

NM-->cholinergic

58

Cholinergic nerves

1. all nerve fibers in somatic nervous system = NM 2. All PRE-ganglionic fibers in ANS (SYMPATHETIC & PARASYMPATHETIC) = NN 3. All POSTganglionic fibers in PARAsympathetic nervous system = M1-3

59

Effect of acetylcholine

DUMBBELSS: D=diarrhea (Smooth muscle contraction & sphincter relax) U=urination (Smooth muscle contraction & sphincter relax) M=miosis (pupil & ciliary muscle contraction*) B=bradycardia (reduce HR, FOC, CO & vasodilation reduces BP) B=bronchoconstriction (Smooth muscle contraction) E=excitation of skeletal muscle L=lacrimation S=secretion S=sweating Sphincters: relaxation smooth muscle contraction EXCEPT in bv->VASODILATION *use for near vision

60

M3 location & effects

1. smooth muscles (GIT, Bronchial, detrussor): contraction-->diarrhea, bronchoconstriction & urination. EXCEPT BV-->vasodilation-->decrease BP due to release of NO 2. Glands--> increase salivation, lacrimation, sweating, gastric acid 3. Pupil--> Miosis-->increase outflow of aqueous humor-->decrease IOP 4. Ciliary Muscle-->contraction 5. Trigone & sphincters-->relaxation-->urination

61

Indirect Cholinergic Agonists

act by inhibiting metabolism of ACh-->increases concentration in synapse-->increases action of ACh

62

Direct Cholinergic agonists examples

1. Acetylcholine (B) 2. Bethanechol (M) 3. Pilocarpine (naturally occurring alkaloid; M) 4. Carbachol (like bethanechol, M&N) 5. Methcholine 6. Nicotine (like pilocarpine, N) Direct cholinergic agonists = bind directly to cholinergic receptors

63

Indirect Cholinergic Agonist Examples

1. Neostigmine (B) 2. Physostigmine (B) 3. Pyridostigmine (B) 4. Edrophonium (B) 5. Tacrine, Donepezil (B) 6. Ecothiophate (B) 7. Malathion, Parathion, Sarin (B) 1-5 are used to treat Myasthenia Gravis, Alzheimers & Glaucoma

64

Woman with: -dry skin. -tiredness and fatigue – which are common and can lead to total exhaustion. -muscle pain. -joint pain, stiffness and swelling. -vasculitis (inflammation of blood vessels)

Sjorgens syndrome

65

Acetylcholine

1. Direct Cholinergic Agonist 2. both Muscarinic & nicotinic actions 3. bc of non-specific actions & rapid inactivation by acetylcholinesterase, this drug has no clinical use 4. Vasodilation by ACh is due to the release of EDRF (endothelium derived relaxing factor, aka NO)

66

Bethanechol DOA; Uses; MOA

1. Direct Cholinergic Agonist 2. strong muscarinic action & little or no nicotinic action 3. orally active, poor lipid solubility 4. DOA = 30m-2h Therapeutic uses: 1. paralytic ileus 2. non-obstructive urinary retention (ie post-op) MOA = stimulates M3 receptors-->increase bowel movements & bladder contraction no N effects

67

DOC for treating paralytic ileus or non-obstructive urinary retention

Bethanechol

68

Pilocarpine Uses; DOA

1. alkaloid 2. Has mucarinic activity only 3. lipid-soluble & penetrates cornea very well 4. DOA = 30m-2h 5. Therapeutic Uses: 1. Glaucoma: due to increased intraocular tension 2. Sjorgens syndrome: chronic, inflammatory autoimmune disorder characterized by dry mouth (xerostomia) & dry eye (keratoconjunctivitis sicca. Works to control these symptoms

69

Drug used to reduce dry mouth

Pilocarpine

70

Drug used to treat Sjorgens syndrome

Pilocarpine

71

Reversible Indirect acting Cholinergic agonists

1. Neostigmine 2. Physostigmine 3. Pyridostigmine 4. Edrophonium 5. Tacrine--used to treat alzheimers 6. Donepezil--used to treat alzheimers These are all short-acting & the enzyme is reactivated and hydrolyzes ACh as usual

72

Irreversible Indirect acting Cholinergic agonists

1. Ecothiophate--used to treat glaucoma 2. Malathion 3. Parathion 4. Sarin These are all long-acting; enzyme reactivation takes extremely long time or almost doesn't take place-->persistent action of ACH in body Ecothiophate is the only one used therapeutically; the rest are insecticides or war gases

73

Physostigmine: Use; MOA

tertiary amine; lipid soluble-->good eye penetration & CNS penetration; used to treat Glaucoma MOA = reversible inhibition of AChE--> increase ACh Used as a TOPICAL treatment in Glaucoma; Causes miosis-->increases outflow of aqueous humor-->decreases IOP reverses the central & peripheral signs of muscarinic blockade

74

Neostigmine

quatrenary amine; lipid INSOLUBLE, NOT used to treat Glaucoma

75

transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness

symptoms of myasthenia gravis Dx = blood ACh receptor antibody level

76

Tx of Myasthenia Gravis

1. AChE inhibitors: Neostigmine, pyridostigmine, edrophonium (these are all reversible) 2. immunosuppressants & corticosteroids 3. Thymectomy (bc thyroid dysfunction worsens symptoms)

77

Neostigmine: use; method given

Reversible AChE Inhibitor used in acute cases of myasthenia gravis; given via IV

78

Pyridostigmine: use; method given

Reversible AChE Inhibitor; has a longer duration of action than neostigmine, so good for maintenance/long term therapy in myasthenia gravis. 2. Given orally

79

Edrophonium: use

Reversible AChE Inhibitor; shortest acting for 5 minutes 2. used in diagnosis of M. Gravis & to differentiate myasthenic & cholinergic crisis by doing a Tension test.

80

Myasthenic Crisis

if drug therapy is inadequate patients develop severe muscle weakness

81

Cholinergic crisis

if excessive amounts of drugs have been used, patients will become paradoxically weak because of nicotinic depolarizing blockade of motor end plate

82

Tensilon test

Used to differentiate myasthenia crisis from Cholinergic crisis. small doses of edrophonium (1-2mg IV) will produce NO RELIEF or even WORSEN weakness if the patient is receiving EXCESSIVE AChE Inhibitor therapy = cholinergic crisis patient will improve with edrophonium if has myasthenic crisis--> may be indication for increase in AChE inhibitor dosage

83

Patient with severe muscle weakness improves with edrophonium given by IV

Patient had myasthenia crisis--> may be indication for increase in AChE inhibitor dosage

84

Patient with severe muscle weakness has no relief when edrophonium given by IV; may even have worsening of symptoms

patient had cholinergic crisis

85

Alzheimers Disease

progressive disorder involving neural degeneration in the cortex leading to a marked loss of memory & of the ability to carry on ADL; MCC of degenerative dementia mostly due to loss of cholinergic neurons, thus mainstay of treatment is ACh therapy; Cause unknown Tx: AChE Inhibitors like Tacrine, Rivastigmine & Donepezil

86

Tx for OP Poisoning

1. Atropine: muscarinic receptor blocker (Anticholinergic drug) given via IV large doses until you observe mydriasis, tachycardia, & dryness of mouth Can't control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn't have any role in reversing the CNS effects of OP poisoning 2. Pralidoxime (2-PAM): AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before "aging of the enzyme" OP antagonist.

87

Treatment for Alzheimers

AChE Inhibitors like Tacrine, Rivastigmine & Donepezil

88

Tacrine

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

89

Rivastigmine

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

90

Donepezil

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

91

fasciculations followed by paralysis

nicotinic toxicity

92

Miosis, blurred vision, bradycardia, salivation, sweating, urination, bronchial constriction, vomiting, diarrhea

symptoms of organophosphate poisoning; mainly due to stimulation of muscarinic receptors Due to phosphorylation (irreversible inhibition) of the enzyme resulting in excess ACh

93

3 cardinal signs of atropinization

mydriasis, tachycardia & dry mouth

94

Pralidoxime (2-PAM)

AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before "aging of the enzyme" OP antagonist.

95

Atropine

muscarinic receptor blocker (Anticholinergic drug) given via IV large doses to treat OP poisoning until you observe mydriasis, tachycardia, & dryness of mouth Can't control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn't have any role in reversing the CNS effects of OP poisoning

96

Features of toxicity of cholinergic drugs (OP poisoning)

DUMBBELSS D=diarrhea, abdominal cramps, vomiting (Muscarinic) U=urination (Muscarinic) M=miosis (Muscarinic) B=bradycardia (Muscarinic) B=bronchospasm (Muscarinic) E=excitation of skeletal muscle (Nicotinic)* L=lacrimation (Muscarinic) S=salivation (Muscarinic) S=sweating (Muscarinic) *Atropine can't fix nicotinic symptoms bc just blocks muscarinic receptor

97

methacholine challenge test

primarily used to diagnose bronchial hyperreactivity = hallmark of asthma & occurs in COPD subject inhales aerosolized methacholine-->bronchoconstriction other therapeutic uses are limited by its adverse cardiovascular effects = bradycardia & hypotension (bc it's a cholinomimetic)

98

Use of Edrophonium

diagnosis of M. gravis

99

Use of neostigmine

Tx of M. gravis acts on cholinesterase; N&M effects

100

43 yo unable to continue picking vegetables: unsteady gait, difficulty speaking, swallowing, blurry vision, watery eyes, tightness in chest-->difficulty breathing

OP poisoning irreversibly inhibits AChEsterase-->increase in ACh Tx with atropine & 2-PAM

101

Use of pyridostigmine

Tx of M. gravis

102

Use of Physostigmine

glaucoma & atropine overdose

103

Malathion, paration

used as insecticides parathion more toxic than malathion. Very lipid soluble & rapidly absorbed through lungs & skin

104

Drugs used to treat paralytic ileus

bethanechol & neostigmine

105

causes miosis (constriction of pupillary sphincter m)

M3

106

opposite of M3 in the blood vessel is

alpha 1

107

increases outflow of aqueous humor-->decreases IOP

M3

108

causes accommodation (contraction of ciliary muscle) for near vision

M3

109

causes mydriasis (pupillary sphincter relaxation)

alpha 1

110

causes urinary retention via sphincter contraction

alpha 1

111

opposite of M3 in the pupil is

alpha 1

112

reduces release of NE & consequences

alpha 2-->bradycardia, hypotension, also causes inhibition of liplysis in fat cells

113

results in bronchodilation

beta 2

114

results in bronchospasm

M3

115

What happens when you increase IP3 & DAG?

Gq-->stimulate PLC-->increase IP3 & DAG--> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity. In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

116

what's the consequence of aldosterone secretion

aldosterone-->kidney tubules to increase sodium & water reabsorption-->increase in blood volume-->increase in BP

117

Opposite of M2 in the heart is

beta 1

118

opposite of M3 in smooth muscle is

beta 2

119

opposite of M3 in sphincters is

alpha 1

120

receptors found on blood vessels

M3 & alpha 1

121

receptors found in smooth muscle

M3 & beta 2

122

receptors found in sphincters

M3 & alpha 1

123

receptors found in pupils

M3 & alpha 1

124

receptors found in glands

M3

125

Receptors found in the heart

M2 & beta 1

126

D1 receptor 1. location 2. MOA 3. effect

1. smooth muscle 2. Gs--> increase cAMP 3. relaxes renal vascular smooth muscle

127

Reflex response to a drop in blood pressure how can you block this response?

increase in sympathetic outflow (-->increase in HR and FOC; from beta 1) and increase renin release (from beta 1; --> increase salt and water retention) and decrease in parasympathetic you can block this with ganglion-blocking drugs i.e. hexamethonium

128

what happens in juxtaglomerular cells when renal blood flow decreases

1. JG cells convert prorenin (found in blood) to renin and secrete it into circulation 2. renin converts angiotensinogen (secreted by liver) to angiotensin 1 3. AT1-->AT2 by ACE (found in lungs) 4. AT2--> BV constriction-->increase in BP 5. AT2 also stimulates secretion of aldosterone from the adrenal cortex 6. aldosterone-->kidney tubules to increase sodium & water reabsorption-->increase in blood volume-->increase in BP

129

DAG modulates

DAG modulates action of PKC

130

IP3 leads to

IP3-->Ca2+ release from intracellular storage-->sm contraction

131

from where is angiotensinogen secreted?

liver

132

where is ACE found

lungs

133

what does AT2 do?

1. AT2-->BV constriction-->increase in BP 2. AT2 also stimulates secretion of aldosterone from the adrenal cortex)

134

from where is aldosterone secreted?

adrenal cortex (AT2 also stimulates secretion of aldosterone from the adrenal cortex)

135

In ANS preganglionic fibers, ACh acts through ___ receptors?

Nn

136

does neostigmine have nicotinic, muscarinic or both activity

both (all indirect, reversible cholinergic agonists do)

137

drug used to treat atropine overdose

physostigmine

138

D1 receptor location

smooth muscle

139

D2 receptor location

nerve endings

140

beta 2 affect on the human liver

activates glycogenolysis

 

bc increases pancreas insulin secretion

141

alpha 2 affect on fat cells

inhibition of lipolysis

142

alpha 1 affect on the prostate

causes contraction in ductus deferens and seminal vesicles -->ejaculation

143

alpha 2 affect on vascular smooth muscle in the nasal mucosa

nasal decongestion

144

beta 2 affect on skeleton muscle

promotes potassium uptake

 

also causes vasodilation of the vascular beds in skeletal muscle which --> decrease in TPR

145

2 ways in which adrenergic system can affect PVR

1. alpha 1-->vasoconstriction-->increases TPR--> increases BP

 

2. beta 2-->vasodilation--> decreases TPR--> decreases BP

146

receptors that act on fat cells and their actions

beta 3: activates lipolysis

 

alpha 2: inhibites lipolysis