9 - Autonomic Control of CVS Flashcards

1
Q

What control does the ANS have over the heart?

A
  • Controls heart rate
  • Controls force of contraction
  • Alters TPR
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2
Q

What nervous input is on the heart at rest?

A
  • Vagal parasympathetic influence
  • Therefore dennervated heart still beats but faster
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3
Q

What is the parasympathetic input to the heart?

A

- Vagus nerve (10th cranial nerve)

  • Synapse at SA or AV node
  • Post ganglionic release ACh that acts on M2 to cause negative chronotropy by slowing firing of SAN and decreased AV node conduction velocity
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4
Q

What is the sympathetic input to the heart?

A
  • Cardiac accelerator nerve
  • Innervate the SA node, AV node and myocardium
  • Act on B1 mainly and have a positive chrontropic and inotropic effect
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5
Q

What part of the brain controls the innervation of the heart?

A

Medulla oblongata

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6
Q

What does sympathetic and parasympathetic innervation do to the pacemaker potential and why?

A
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7
Q

How does the sympathetic nervous system increase the force of contraction of the heart?

A
  • Noradrenaline released which acts on B1 receptors

- Increase in cAMP and PKA

- PKA phosphorylates Ca channels, increasing Ca entry from outside and SER on plateua of AP

  • Also PKA increases uptake of Ca into the SER so more released with each AP
  • More Ca, increased force of contraction
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8
Q

How does the sympathetic nervous system change the total peripheral resistance?

A
  • Most arteries and veins have sympathetic innervation of a1 adrenoreceptors
  • Skeletal and coronary mucle also have b2 receptors
    (exception: erectile tissue has parasympathetic innervation)
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9
Q

What is vasomotor tone?

A
  • Blood vessels always have some sympathetic innervation to give tone to the smooth muscle
  • To constrict and dilate the sympathetic response increases and decreases
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10
Q

What hormones act on the adrenoreceptors in blood vessels?

A
  • b2 and a1 in skeletal, myocardium, liver
  • Noradrenaline from SNS on a1 causing vasoconstriction

- Circulating adrenaline on b2 causing vasodilation as adrenaline has higher affinity for b2

  • At higher concentrations a1 are activated by adrenaline
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11
Q

Why does vasodilation occur in b2 receptors and vasoconstriction in a1?

A

b2 - PKA produced which opens K channels and inhibits MLCK

a1 - Stimulates IP3 production. Increase in calcium concentration from stores and from extracellular so vasoconstriction

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12
Q

What is responsible for adequate perfusion of skeletal and coronary muscle?

A

Local vasodilator, e.g K+ and H+ from active tissue metabolism

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13
Q

What are the names of the receptors on both sides of the circulatory system?

A
  • Baroreceptos
  • Atrial receptors
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14
Q

What is the baroreceptor reflex?

A
  • Blood pressure increases, stretches the nerve endings, opening ion channels and firing more A.P’s

- Carotid Sinus: Glossopharyngeal Nerve

- Aortic Arch: Vagus Nerve

When the medulla oblongata recieves innervation, it changes the sympathetic and parasympathetic outflow to change TPR, heart rate, and force of contraction

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15
Q

What is the short term response to hypertension?

A

Baroreceptor reflex

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16
Q

What are sympathomimetics?

A
  • Agonists
    e. g adrenaline in cardiac arrest/anaphalaxis , dobutamin in cardiogenic shoc, salbutamol
17
Q

What are some adrenoreceptor antagonists for hypertension?

A

- Praxosin (a1): not first line. causes vasodilation on vessels

- Propanolol (B1/B2): helps atrial fibrillation. slows heart rate and reduced force of contraction

- Atenolol (selective B1): less risk of bronchoconstriction

18
Q

What are cholinergics?

A
  • Muscarinic agonists and antagonists
  • e.g pilocarpine (agonist) to allow drainage of humour
  • e.g atrophine (antagonist) to increase HR, bronchial dilation
19
Q

What would happen if you dennervated the heart?

A

Would beat faster as not under vagal innervation like it normally is at rest

20
Q

Describe the role of the renin-angiotensin-aldosterone system in the long term control of blood pressure.

A

Renin is released from the kidneys in response to reduced aBP. Renin cleaves angiotensinogen to angiotensin I. Angiotensin I is not physiologically active but is further cleaved to angiotensin II by Angiotensin Converting Enzyme (ACE). Angiotensin II promotes aldosterone release from the adrenal cortex. Aldosterone promotes sodium and water retention by the kidneys.

Angiotensin II is also a powerful vasoconstrictor. This increases TPR.