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Regulation of cardiovascular :
Adaptation to short-term changes is provided by the Frank-Starling mechanism. Long-term changes in cardiac activity are regulated by the autonomic nervous system.
1. Frank-Starling mechanism:
     Definition:
a law that describes the relationship between end-diastolic volume and cardiac stroke volume Cardiac contractility is directly related to the wall tension of the myocardium.
  • An increase in end-diastolic volume (preload) will cause the myocardium to stretch (↑ end diastolic length of cardiac muscle fibers), which increases  contractility (↑ force of contraction) and results in increased stroke volume in order to maintain cardiac output.
This relationship between end-diastolic volume and stroke volume is shown in the Frank-Starling and stroke volume is shown in the Frank-Starling curve. and stroke volume is shown in the Frank-Starling
curve.
  1. Aim:

 Maintain CO by modulating contractility and SV Stroke volume of both ventricles should remain the same.

 Autonomic innervation : The autonomic nervous system is able to regulate heart rate, excitability, conductivity, relaxation, and contractility. 
  1. Sympathetic fibers

innervate both the atria and ventricles.

Parasympathetic fibers 
only innervate the atria.


Definition:


modulation of cardiac action by sympathetic and/or parasympathetic nerve fibers

Function: 


long-term regulation of cardiac action
Chronotropy: any influence on the heart rate
Dromotropy: any influence on the conductivity of myocardium
Inotropy: any influence on the force of myocardial contraction
Lusitropy: any influence on the rate of relaxation of the myocardium
Bathmotropy: any influence on the excitability ofof the myocardium
Bathmotropy: any influence on the excitability of the myocardium.

   A. Sympathetic effect :
On :
a. Atria and ventricles : Fibers from the sympathetic cervical trunk (superior, middle, and
inferior cardiac nerve).
It increase the heart rate, conduction, contractility and relaxation.
  The mechanism :
    Activation of beta1 adrenergic receptors (Gs protein-coupled) of the heart by epinephrine and
norepinephrine → ↑ activity of adenylyl cyclase → ↑ intracellular cAMP concentration in SA node
cardiomyocytes, which then:

1. Increases the conductance of funny sodium channels and L-type calcium channels → ↑ influx
of cations during spontaneous depolarization → faster attainment of the threshold potential
during phase 4 of pacemaker action potential for initiating the rhythmic cardiac action potential →
↑ heart rate (positive chronotropic)

 2 . Activates protein kinase A , which leads to two effects:
  •  Phosphorylation of L-type Ca2+ channels in AV node → increased Ca2+ entry → increased Ca2+-induced Ca2+ release during action potential → increased contraction and conduction (positive dromotropic and inotropic)
  •  Phosphorylation of phospholamban → activation of sarcoplasmic reticulum Ca2+- ATPase (SERCA) → increased transport of Ca2+ back into sarcoplasmic reticulum after a contraction → faster relaxation (positive lusitropic).

       B. Parasympathetic effect :
 On:
 Atria : Branches of the vagus nerve
  • Cervical cardiac branches
  • Thoracic cardiac branches

It decrease the heart rate and atrial contractility.
  The Mechanism :
  •  Exerts its action on the heart through parasympathetic muscarinic ACh receptors
  •  Exerts its action on the heart through parasympathetic muscarinic ACh receptors (subtype M2) on SA and AV node cardiomyocytes.
  • Activation of M2 receptors on SA node (negative chronotropic).
  • Reduces the conductance of funny sodium channels via adenylyl cyclase, decreasing cAMP → ↓ pacemaker current (lengthens the rate of depolarization in the slow depolarization phase).
  •  Increases conductance of the slow potassium channels → hyperpolarization of the resting membrane potential (harder to overcome).
  •  Vagal fibers innervate the AV node (negative dromotropic): slows cardiac action potential propagation (can result in complete AV block).


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