L6.1 Hormonal control of cardiac function Flashcards Preview

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Flashcards in L6.1 Hormonal control of cardiac function Deck (14):
1

Features of adrenaline

  • SNS hormone → stimulates heart functions
  • Secreted from adrenal medulla (modified sympathetic ganglion)
    • Release A into blood stream (No post ganglion neurons)

2

Overview of the SNS receptors

3

Inotropic and chronotropic

  • Inotropic = affects contractility 
  • Chronotropic = Affects HR

4

How do b1 cardiomyocytes increase contractility

 

  • Increase L&T type Ca current
  • Increase SR Ca release channels
  • Increase Ca transient via PKA
  • Increase Ca ATPase (SERCA)

 

5

Mechanism of b1

  • Acts via Gas → adenyl cyclase → cAMP → PKA → phosphorylates proteins → regulation
    • Increase Ca transients → more rapid relaxation

6

Mechanism of a1

  • (Increase Ca sensitivity)
  • Gq protein → splits subunits → PLC (uses membrane as signaling process)
    • PLC catalyses: PIP2 → DAG + IP3 (For nuclear transcription/SA node function)
    • DAG → PKC activation → increase pH → increase myofilament Ca sensitvity

7

What is the effect of pH

  • Alkaline pH shifts induces forces increase
  • Ca & pH effects are additive

8

a vs b inotropic effects

  • b > a Ca transient
    • Ca transient occurs before twitch
  • b1 stimulates increase force by 20% & Ca transient by 400%
  • a has greater contraction value for less Ca load
  • BUT b contractions is faster than a
    • Increase time to ventricle to relax → Increase time for ventricle to fill → Increase SV in next pump

9

Vasoconstrictor inotropic agents: Endothelin-1

  • Inotropic
  • But when systematically → Decrease O2 supply to heart → Decrease contractility 
  • Produced from:
    • Endocardial & Endothelial cells
    • Fibroblasts

 

10

Vasoconstrictor inotropic agents: ANGII

  • PKC >> PKA → Increase sensitivity (Na/H) & Ca entry (Ca channels)
  • Systemically infused → vasoconstrictor → Decrease O2 supply to heart and hence decrease contractility
  • BUT enhances contractility when applied to isolated heart muscles
  • Produced from:
    • Endocardial & endothelial cells
    • Fibroblasts + CARDIOMYOCYTES

11

Local or distal actions of ET1 & ANGII?

  • Both endothelin and ANG II are primary LOCAL mediators (spillovers into circulation → SE)

12

Intracardiac functional role of ANGII

  • Too much ANG II → earlier mortality
  • Acute ANG II → Increase pump functions
  • Chronic ANG II → Decrease pump function (due to hypertrophy leading to decompensation)

13

When are ET-1 and ANGII produced/

Produced and released in heart in response to stretch and growth factors

14

ANF

  • -ve inotropic
  • Synthetised & released by atrial myocyte (responds to stretch)
  • Relief strain on heart muscles (cardiomyocyte relaxation)
  • Binds & activates guanylyl cyclase activity (Converts GTP to cGMP → activating PKG)
  • Promotes H2O & Na excreted → Decrease BV (renal vasodilation)
  • Induces relaxation → Decreases Ca current & Increase SR Ca ATPase