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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 ca2+

A

cytotoxic (hypercontraction)

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3
Q

what is the concentration of cytosolic (intracellular) calcium

A

100nM (10^-7 M)

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4
Q

what is the concentration of extracelluar calcium

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 intracellular calcium stores

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7
Q

what are 5 calcium entry mechanisms

A

ligand gated,
voltage gated,
store operated calcium channels, GPCRs, and ryanodine receptors

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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 and 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

name 3 voltage gated Ca2+ inhibitors

A

verpamil
diltiazem
dihydropyridines (nifedipine)

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13
Q

what does verapamil do

A

block voltage gated calcium channels

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14
Q

what are dihydropyridines? give an example

A

type of voltage gated Ca2+ channel blocker
nifedipine

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15
Q

what does nifedipine do

A

type of dihydropyridines, blocks voltage gated Ca2+ channels

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16
Q

what is diltiazem?

A

inhibitor of voltage gated Ca2+ channels

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17
Q

what are verapamil, diltiazem and dihydropyridines (nifedipine) used for?

A

angina hypertension and some cardiac dysrhythmias by reducing contraction of vascular smooth muscle

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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

can cause so much Ca2+ entry the cell dies

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20
Q

what are ATP-gated P2X channels?

A

only true ligand gated ion channel in smooth muscle, very calcium 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

calcium release activated channel

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23
Q

how do SOC and CRAC increase intracellular store (mechanism)

A

Depletion of Ca(2+) from the ER causes STIM (calcium sensing proteins) to accumulate at ER-plasma membrane (PM)
-physical interactions allows CRAC channels to open

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24
Q

what are 3 calcium extrusion mechanisms

A

PMCA (plasma membrane calcium ATPase)
NCX sodium calcium exchanger
SERCA (sarcoplasmic endoplasmic reticulum calcium ATPase)

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25
Q

what does Ca2+ ATPase get energy from

why does it need energy

A

atp hydrolysis (transport across concentration gradients)

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26
Q

what does the plasma membrane PMCA pump do

A

keep cytoplasmic Ca2+ low by pumping it out of the cell (type of Ca2+ ATPase)

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27
Q

what does the SERCA pump do

A

keep cytoplasmic Ca2+ low by pumping it into ER or SR (type of ATPase)

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28
Q

what does thapsigargin do

A

block SERCA pump, can cause contraction due to increased intracellular calcium)

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29
Q

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

A

brings 3 Na+ in and 1 Ca2+ out

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30
Q

how does NCX get energy

A

couples the flow of 3 Na+ ions down their EC into the cytosol to the move 1 Ca2+ ion out of the cell against its concentration gradient

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31
Q

where is the NCX

A

on plasma membrane

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32
Q

where is PMCA

A

on plasma membrane

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33
Q

why can NCX cause depolarization?

A

the transporter is elecrogenic (it causes the net movement of 1 positive charge inward, since it moves 3 Na+ in and 1 Ca2+ out)

34
Q

describe reverse mode NCX activity

A

caused by a reduction in the Na+ concentration gradient
if the concentration of Na+ in the cell is too high, it will action case Na+ to leave the cell and bring Ca2+ in

35
Q

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

A

inositol tris phosphate receptor (GPCR)
ryanodine receptor (calcium induced calcium release)

36
Q

what does the IP3 receptor do

A

ligand gated ion channel in the SR/ER that is activated by IP3
results in activation of Gq signalling and elevation of intracellular calcium (and DAG –> PKC)

37
Q

what does RYANODINE do

A

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

38
Q

what kind of ryanodine receptor is involved in skeletal muscle contractions

A

RyR1

39
Q

what kind of ryanodine receptor is involved in cardiac muscle contractions

A

RyR2

40
Q

what does ryanodine receptors do to ca2+ release in cardiac muscle? mechanism?

A

CICR (calcium induced calcium release)
Ca2+ acts on RyR to release Ca2+ from the ER/SR

41
Q

what does CAFFEINE do?

A

sensitizes ryanodine receptor and causes Ca2+ release from ER SR at physiological Ca2+ concentrations
sensitizes muscle to contract more
stimulant

42
Q

what does dantrolene do

what is it similar to

A

blocks RyR (like ryanodine does at high conc)

43
Q

what is dantrolene used for

A

malignant hyperthermia caused by genetic RyR abnomalities or anesthesia
mutations cause RyR to be oversensitive, resulting in too much intracellular calcium, too much heat release and hyperthermia

44
Q

what is calmodulin

A

ca binding protein that activates many effectors

45
Q

what is the main downstream effector for calmodulin

A

CaM kindase

calcium calmodulin kinase

46
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
47
Q

Is na higher on inside or outside

A

outside

48
Q

Is k higher on inside or outside

A

inside

49
Q

Is Cl higher on inside or outside

A

varies, but higher outside

50
Q

what determines resting membrane potential

A

resting K channels (selectively K permeable)

51
Q

what is the normal resting membrane potential determined by K+

A

-40 to -80 mV

52
Q

which three ion pumps are primarily responsible for controlling ion concentrations within the cell?

A

NaK ATPase and Ca ATPase and NCX)

53
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)

54
Q

what does digoxin do and what is its drug class

A

digitalis cardiac glycosides, blocks Na K ATPase

55
Q

what happens in action potential (2 main things)

A

threshold stimulus causes opening of voltage gated Na+ channels, rapid influx of Na+, followed by inactivation of Na+ channels and delayed outward flux of K+ results in repolarization

56
Q

what causes the refractory period

A

inactivation of Na channels

57
Q

is the AP and depolarization mechanism same in all tissues

A

no, varies per tissue. complex in heart

58
Q

what do drugs that cause depolarization do to excitability

A

increase

59
Q

what do drugs that cause hyperpolarization do to excitability

A

decrease

60
Q

what does a stronger depolarizing stimulus do to AP

A

increases # of them

61
Q

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

A

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

62
Q

what causes contraction of muscle

A

interaction between actin and myosin fueled by ATP and initiated by increase in intracellular Ca
interaction is inhibited, by troponin, MLCK

63
Q

what does ACh at nAChR do

A

causes depolarization (excitatory junction potential)

64
Q

decribe the steps of skeletal muscle contraction

A

ACh activated nAChRs, resulting in depolarization
AP propogates thru T-tubules, activating L-Type Ca2+ channels (aka dyhydropyridine receptors)
Mechanical stimulation of RyR1 receptors on the ER/SR, causing Ca2+ release
Ca2+ release binds troponin, removing it from myosin binding site on actin
Muscle contraction!

65
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

66
Q

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

A

L-type dihydropyridine ca receptors and RyR1

67
Q

what happens in skeletal muscle once ca is release

A

ca binds to troponin

68
Q

what does troponin do

A

stops interaction between actin and myosin

69
Q

what happens when ca binds to troponin

A

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

70
Q

what kind of tissue is myogenic and what does it mean

A

heart because it does not need stimulus to start contraction

71
Q

describe cardiac muscle contraction

A

Change in voltage results in opening of L-type Ca2+ channels
Ca2+ causes activation of Ryr2 to release Ca2+ from the ER/SR
CICR
Contraction!

72
Q

what receptor in heart is activated by AP

A

L-type Ca2+ receptors (voltage gated)

73
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

74
Q

describe the difference between skeletal and cardiac muscle contraction

A

skeletal needs L type and ryanodine to be beside each other
heart doesn’t (L type releases calcium which stimulates RyR)

75
Q

what makes smooth muscle contraction different than heart and skeletal

A

no troponin!!!

76
Q

if smooth muscle lacks troponin, what causes contraction?

A

myosin light chain kinase

77
Q

what do agonists working through Gq do to smooth muscle

A

contract (alpha 1)

78
Q

what do agonists working through Gs do to smooth muscle

A

relax (beta 2)

79
Q

what does NO do to smooth muscle

A

relax (guanylyl cyclase)

80
Q

what does cAMP do in the smooth muscle contraction pathway and how?

A

inactivate MLCK by phosphorylating it (double phosphorylation)
INHIBITS CONTRACTION/CAUSES RELAXATION

81
Q

what does cGMP do to smooth muscle pathway contraction pathway and how?

A

dephosphorylating myosin-LC-PO4
INHIBITS CONTRACTION/CAUSES RELAXATION

82
Q

what does Gq signalling do to smooth muscle contraction and how?

A

intracellular Ca2+ release –> activated Ca2+ calamodulin –> activate MLCK –> phosphorylated myosin-LC –> contraction

PMCOL 343 (31 decks)

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