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PMCOL 343 > 1-cardio > Flashcards

1-cardio Flashcards

1
Q

what is Ca2+ important for

A

contraction
excitation
secretion

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2
Q

what happens with high intracellular ca

A

toxic

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3
Q

what is free intracellular calcium levels at usually (#)

A

100nM (10^-7 M) (0,1 micro molar)

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4
Q

what is extracellular calcium levels at usually (#)

A

2mmolM (2.5^-3 M)

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5
Q

where is calcium stored

A

ER and SR and mitochondria

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6
Q

what are calcium sparks

A

localized release of calcium

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7
Q

what are 3 calcium entry mechanisms

A

ligand gated,
voltage gated,
store operated calcium channels

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8
Q

when do voltage gated ca channels open

A

when cell is depolarized

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9
Q

what are the types of voltage gated ca channels

A

LNPRT (Cav1=L, Cav2= NPR, cav3=T)

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10
Q

where are N and P calcium channels and what do they do

A

neuronal so invovled in NT release

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11
Q

where are L type calcium channels

A

heart and smooth muscle

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12
Q

what does verapamil do

A

block L type calcium channels

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13
Q

what are dihydropyridines and what is a type of one

A 
class of drug
nifedipine
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14
Q

what does nifedipine do

A

block L type calcium channels

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15
Q

what do dihydropyridines do

A

block L type calcium channels

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16
Q

what are dihydropyridines (nifedipine) and verapamil used for

A

angina hypertension and some cardiac dysrhythmias

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17
Q

when are ligand gated channels activated and what does it cause

A

when NT or other agonists cause Ca influx

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18
Q

what is an example of a highly permeable Ca ligand gated channel

A

NMDA glutamate channels

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19
Q

what can be an issue with ligand gated channels

A

too much ca entry can kill (like too much glu excites them to death)

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20
Q

what are ATP-gated P2X channels and whats the big deal with them

A

only true ligand gated ion channel in smooth muscle

-highly ca permeable

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21
Q

what type of channel is the CRAC channel

A

store operated calcium channel

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22
Q

what does CRAC channel stand for

A

ca release activated Ca

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23
Q

when do SOC and CRAC channels dp

A

allow ca entry when intracellular stores are depleted (ER SR)

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24
Q

how do SOC and CRAC increase intracellular store (mechanism)

A

STIM1 accumulates where ER is juxtaposed to the plasma membrane
-physical interactions allows CRAC channels to open

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25
Q

what are 3 calcium extrusion mechanisms

A

PMCA-plasma membrane NCX-calcium ATPase
sodium calcium exchange
SERCA sarcoplasmic endoplasmic reticulum calcium ATPase

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26
Q

what is the main role of calcium extrusion mechanisms

A

keep ca in cell low by pumping it into ER or out of cell

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27
Q

what does ca atpase get energy from

why does it need energy

A

atp hydrolysis (transport across concentration gradients)

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28
Q

what does the plasma membrane PMCA pump do

A

keep cytoplasmic ca low by pumping it out of the cell

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29
Q

what do PMCA pumps require

A

energy from ATP hydrolysis

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30
Q

what does the SERCA pump do

A

keep cytoplasmic ca low by pumping it into ER or SR

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31
Q

what does thapsigargin do

A

block SERCA pump

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32
Q

what does the NCX Na-Ca exchange do (which molecules how many and where)

A

brings 3 na in and 1 ca out

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33
Q

how does NCX get energy

A

uses the Na gradient to get energy (brings na inside like its gradient wants it to) to get ca out

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34
Q

where is the NCX

A

on plasma membrane

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35
Q

where is PMCA

A

on plasma membrane

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36
Q

what kind of exchanger is NCX (special word we learned)

A

electrogenic because it causes depolarization by net inward movement of positive charge

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37
Q

what transporter is involved in generating AP in many regions of heart

A

NCX

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38
Q

what transporter is electrogenic

A

NCX

and NaK ATPase

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39
Q

how does a reduced na gradient affect intracellular Ca2+ and why

A

accumulation inside because it needs the gradient to let it leave

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40
Q

what are 2 transporters that do exchange between ER SR and cytosol

A 
inositol tris phosphate receptors (IP3R)
ryanodine receptor (RyR)
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41
Q

what does the IP3 receptor do

A

activates ca release from SR ER

42
Q

what kind of channel is IP3 receptor

A

ligand gated

43
Q

where is the ip3 receptor

A

ER SR

44
Q

what kind of mechanism causes ip3 to elevate ca

A

Gq

45
Q

what activates inositol trisphopshate receptor

A

IP3

46
Q

what does RYANODINE do

A

activates RyR at low concentrations (nanomolar) but closes them at high concentrations (micromolar)

47
Q

what kind of ryanodine receptor is involved in skeletal muscle contractions

A

RyR1

48
Q

what kind of ryanodine receptor is involved in cardiac muscle contractions

A

RyR2

49
Q

what does ryanodine receptors do to ca release

A

increase - ca induced ca release from ER SR

50
Q

what kind of receptor causes ca induced ca release

A

ryanodine receptor

51
Q

what does CAFFEINE do to what receptor

A

sensitizes ryanodine receptor and causes ca release from ER SR at physiological ca concentrations

52
Q

what does dantrolene do

what is it similar to

A

blocks RyR (like ryanodine does at high conc)

53
Q

what is dantrolene used for

A

malignant hyperthermia (happens in surgery) due to genetic RyR abnomalities

54
Q

what is calmodulin

A

ca binding protein that activates many effectors

55
Q

what are 2 protein characteristics for calmodulin

A

dimer

4 ER hand binding domains for ca

56
Q

what is the main downstream effector for calmodulin

A

CaM kindase

calcium calmodulin kinase

57
Q

what are some molecular targets for ca

A 
enzymes
kinases
phosphatases
transcription factors
synaptic vesicle proteins (NT release)
contractile proteins
ca binding proteins as intermediate
ca sensitive ion channels
58
Q

Is na higher on inside or outside

A

outside

59
Q

Is k higher on inside or outside

A

inside

60
Q

Is ca higher on inside or outside

A

outisde (very low inside)

61
Q

Is Cl higher on inside or outside

A

varies, but higher outside

62
Q

what determines resting membrane potential

A

resting K channels (selectively K permeable)

63
Q

what is the normal resting membrane potential determined by K+

A

-40 to -80 mV

64
Q

what causes ionic concentrations to be set

A

ion pumps (NaK ATPase and Ca ATPase and NCX)

65
Q

how many na and k pumped and where in NaK ATPase

A

2 K in

3 Na out

66
Q

does Na K pump cause hypo or hyper polarization and why

A

hyperpolarization because it makes the inside more negative (3 na out 2 k in)

67
Q

what does digoxin do and what is its drug class

A

digitalis cardiac glycosides, blocks Na K ATPase

68
Q

is Na K Atpase electrogenic

A

yes

69
Q

what is Na concentration inside and outside

A

inside 12mmol

ouside 145mmol

70
Q

what is K concentration inside and outside

A

150 inside

2.4 outside

71
Q

what is Ca concentration inside and outside

A

0.1 micro inside

2mmol outside

72
Q

what is Cl concentration inside and outside

A

5mmol inside

125mmol outside

73
Q

what happens in action potential (2 main things)

A

depolarization causes opening of Na+ channels to bring Na+ inside
then slower outward K+ flux to end AP

74
Q

what causes the refractory period

A

inactivation of Na channels

75
Q

is the AP and depolarization mechanism same in all tissues

A

no, varies per tissue. complex in heart

76
Q

what do drugs that cause depolarization do to excitability

A

increase

77
Q

what do drugs that cause hyperpolarization do to excitability

A

decrease

78
Q

what does a stronger depolarizing stimulus do to AP

A

increases # of them

79
Q

what is the classical pharmacology method to seeing drug effects of muscle contraction

A

take contractile tissue and put into organ bath
add drug
monitor contractions with transducer

80
Q

what causes contraction of muscle

A

interaction between actin and myosin fueled by ATP and initiated by increase in intracellular Ca

81
Q

what does ACh at nAChR do

A

causes depolarization (excitatory junction potential)

82
Q

what happens when excitatory junction potential reaches threshold

A

generates muscle AP (open Na+ channels)

83
Q

What kind of receptor in skeletal muscle is activated by voltage

A

L-type dihydropyridine ca receptors

84
Q

what happens when L-type dihydropyridine ca receptors are activated in skeletal muscle

A

RyR1 receptors on adjacent ER/SRcome close to L-type dihydropyridine ca receptors to activate Ca release

85
Q

what 2 receptors need to be together to cause ca release in skeletal muscle

A

L-type dihydropyridine ca receptors and RyR1

86
Q

what happens in skeletal muscle once ca is releasd

A

ca binds to troponin

87
Q

what does troponin do

A

stops interaction between actin and myosin

88
Q

what happens when ca binds to troponin

A

stops troponin blocking interaction by actin and myosin so that you can have contraction

89
Q

what kind of tissue is myogenic and what does it mean

A

heart because it does not need stimulus to start contraction

90
Q

what receptor in heart is activated by AP

A

L-type ca receptors

91
Q

what happens when L-type ca receptors are activated in heart (2 things)

A

releases ca

and that ca activates RyR2 to release ca from ER SR

92
Q

what is different with skeletal and cardiac muscle contraction

A 
skeletal needs l type and ryanodine to be beside eachother
heart doesnt (2 type releases calcium which stimulates ryan)
93
Q

does RyR2 and L type need to touch to release ca in heart

A

no

ca from L type stimulates RyR2

94
Q

what makes smooth muscle contraction different than heart and skeletal

A

no troponin!!!

95
Q

what causes contraction in smooth muscle- what is the main thing

A

myosin light chain kinase

96
Q

what do agonists working through Gq do to smooth muscle

A

contract (alpha 1)

97
Q

what do agonists working through Gs do to smooth muscle

A

relax (beta 2)

98
Q

what does NO do to smooth muscle

A

relax (guanylyl cyclase)

99
Q

what does cAMP do in the smooth muscle pathway and how

A

inactivate MLCK by phosphorylating it

INHIBIT CONTRACTION

100
Q

what does cGMP do to smooth muscle pathway and how

A

dephosphorylating myosin LC PO4

INHIBIT CONTRACTION

PMCOL 343 (31 decks)

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