Lecture 4 – Cardiac contraction

Question 1

Rise in ca2+ (5)

Answer 1

FLASH CARD

Question 2

Myosin- actin interactions (5)

Answer 2

Notes

Question 3

Troponin (4)

Answer 3

TnT - tropomyosin
TnI - actin filaments
TnC - ca2+

TnI/TnT- important blood plasma markers for cardiac cell death.

Question 4

decrease in ca2+ and relaxation (5)

Answer 4

FLASH CARD

Question 5

2 things moderate extent of the heart beat (2)

Answer 5

extrinsic control

intrinsic stretch

Question 6

Control of cardiac contractility (2)

Answer 6

Drugs can
1) Increase VGCC activity - Sympathetic mimetic - NA acts on B1, increasing sensitivity of the VGCC. HR increases, then contractility.

2) Reducing Ca2+ extrusions - Glycosides, digitalis. Positive inotropes - increase energy/strength of contraction.
SNS - NA on b1 increases contractility.

Question 7

Cardiac glycosides (3)

Answer 7

Positive inotropic action - inotropes
Digoxin increases contractility by reduced calcium extrusion
Chronic heart failure not anymore due to side effects

Question 8

Cardiac glycosides digoxin process (4)

Answer 8

Digoxin inhibits sodium potassium pump
Increases sodium conc
Less ca extrusion by sodium/calcium exchanger
More calcium uptake into stores means more cicr

Question 9

Other inotropic agents (2,2,2)

Answer 9

Dopamine/dobutamine- B1 stimulants - acute heart failure.
Glucagon- Gs pathway increases cAMP. Acute heart failure.
Amrinone- phosphodiesterase inhibitor, PDE 3. Converts cAMP into AMP reducing PKA and contractility. Used in severe cases - heart transplant .