Drug interactions

Question 1

tetracaine

Answer 1

inhibited by na+ current better at higher ph

Question 2

benzocaine

Answer 2

inhibited na+ better at equal ph values

Question 3

RAC-421 and QX-314

Answer 3

quaternary anaesthetics used by Hille determine whether the uncharged or charged form of the drug was acting

Question 4

Lidocaine

Answer 4

antagonist used to inactivate the channels

Question 5

Tetrodotoxin

Answer 5

• highly selective reversible blockers of VG na+ sodium channels.
• does not affect voltage dependence or inactivation
• binds to COOH residues in the pore and residues correspond to Glu387 in S6

Question 6

Batrachotoxin

Answer 6

• acts on intracellular portions of channel, prevents inactivation and moves activation potential to more negative values
• channel opens far more readily than without the toxin

Question 7

Scorpion toxins

Answer 7

• various toxin
• acts on outside of VG Na+ channels to inhibit inactivation
• acts alongside batrachotoxin

Question 8

classes of drugs acting calcium channels

Answer 8

dihydropyridines, phenylalkylamines, benzothiazepines

Question 9

Dihydropyridines

Answer 9

nifedipine, acts on S6 domain IV and part of the S5-6 loop in domain III

Question 10

Phenylalkylamines

Answer 10

verapamil, acts on S6 part of the S5-6 loop in domain IV

Question 11

Benzothiazepines

Answer 11

diltazem - blocks from the outside, modulate dihydropyridine binding

Question 12

Spermine

Answer 12

intracellular polyamine accounts for occlusion producing rectification

Question 13

Ina

Answer 13

produced by VGna, responsible for depolarising phase of action potential

Question 14

Ica-L

Answer 14

produced by L-type Ca2+, main current during the plateau

Question 15

Ica-T

Answer 15

produced by T-type ca2+ channels and present in nodal and conductive

Question 16

Ina-ca

Answer 16

• electrogenic activity of the na+/ca2+ exchanger
• this serves to remove ca2+ from the cell which has entered through ca2+ channels during the plateau
• activity is affected indirectly by cardiac glycosides, used to treat heart failure

Question 17

Ito1 and Ito2

Answer 17

produced by vg K+ channels. they reactivate rapidly in phase 0, inactivate rapidly.
this activates and inactivates behaviour gives the current its name of transient outward
- responsible for the small notch of the action potential that constitutes phase 1

Question 18

iks

Answer 18

• delayed rectifier current properties.
• that means it activates with a delay after depolarisation with little or no inactivation
• contribute outward current during plateau and thus control the timing of depolarisation
• result of KCNE1 and KvLQT2

Question 19

ikr

Answer 19

• delayed rectifier

- mutations can cause long QT syndrome

Question 20

ikur

Answer 20

• third delayed rectifier

Question 21

Ikp/icl

Answer 21

ikp is a plateau current, shows no rectification or voltage sensitivity
icl is the chloride current, channel responsible for icl is probably CFTR

Question 22

Ik1

Answer 22

• inward rectifier stabiliser the resting potential and preventing k+ loss.
• ikach and ikatp and produce the same sort of current

Question 23

if

Answer 23

pacemaker current