nervous and hormonal control of vascular tone Flashcards

1
Q

describe the depolarization that occurs at varicosities in blood vessels

A
  1. An action potential moves down the axon and arrives at a varicosity.
  2. Depolarisation at the varicosity activating voltage-gated Ca2+ channels.
  3. Influx of calcium causes a release of neurotransmitters - mainly noradrenaline.
  4. NA diffuses to the vascular smooth muscle cells where it binds mainly α1 – contraction; some α2 – contraction and β2 – relaxation. Modulation of responses in both constriction and dilatation.
  5. The noradrenaline is then taken up again and recycled or broken down.
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2
Q

what are sympathetic vasoconstrictor veins controlled by?

A

brainstem

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3
Q

what does tonic mean?

A

1 action potential per second
sets vascular tone

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4
Q

what are the main roles of sympathetic vasoconstrictor nerves?

A

Distinct sympathetic pathways innervate different tissues:
Switching on vasoconstriction in some vessels and off in other vessels (producing vasodilation) eg. exercise increases sympathetic nerve stimulation to GI (less blood flow), and reduces sympathetic nerve stimulation to the skin (more blood flow, to assist heat loss).

Control resistance arterioles:
changes in vascular tone regulated TPR which directly affects blood pressure. Vascular tone helps keep BP stable under different conditions (e.g., standing up, exercising)

pre-capillary vasoconstriction:
less blood enters capillaries - BP drops and insititial fluid moves into the capillary. helps maintain blood volume this is crucial in hypovolemia ( low blood volume) as it temporarily boosts plasma volume to maintain stability

vasoconstriction:
when veins contract they push more blood back to the heart. the heart fills up more before it pumps. the more the heart fills the more it contracts increasing the amount of blood pumped out. higher cardiac output.

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5
Q

when does vasodilation usually occur?

A

occurs when vascular tone produced by sympathetic vasoconstrictor nerves is inhibited.

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6
Q

describe how Nitric oxide is released and what it does

A
  • Some blood vessels are innervated by parasympathetic cholinergic fibres (eg. coronary vessels).
  • These release acetylcholine (Ach) which binds to muscarinic receptors on the smooth muscle and/or endothelium.
  • M3 receptors located on the vascular endothelium can couple to the formation of nitric oxide (NO) causing vasodilation.
    *ACh also causes contraction of smooth muscle via M2 and M3 receptors but this effect is usually less predominant than the NO effect.
  • Cerebral arteries appear to have M5muscarinic receptors that vasodilate in response to ACh.
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7
Q

name and describe some parasympathetic vasodilators

A

Salivary glands – release acetylcholine (Ach) vasoactive intestinal peptide (VIP)

Pancreas & intestinal mucosa – release VIP
Both these tissues need high blood flow to maintain fluid secretion.
Ach/VIP tact on endothelium cause release of nitric oxide (NO) - vasodilatation

Male genitalia (erectile tissue) – release NO
Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilatation.

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8
Q

name and describe some sympathetic vasodilators

A
  • Skin release Ach/VIP causing vasodilatation via NO associated with sweating – increased blood flow causes more sweat and also allows heat loss via skin.
  • Sympathetic activity vasoconstriction would only reduce blood flow, limit sweat production and limit cooling.
  • Emotional centres in brain have some control over these fibres, head, face, upper chest, involved in blushing.
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9
Q

describe sensory vasodilator fibers

A
  • nerves that cause blood vessels to widen
    *sensory nerves
  • when stimulated they release substances such as substances P and CGRP
  • substances relax blood vessel walls increasing blood blow to area.
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10
Q

describe adrenaline (epinephrine)

A
  • Adrenaline is released from the adrenal medulla – via the action of acetylcholine on nicotinic receptors during:
    Exercise
    Flight-Fight-Fear response (increase sympathetic drive)
    Hypotension (baroreceptor reflex)
    Hypoglycaemia
    Main roles – metabolic and CVS effects:
  • Glucose mobilisation (skeletal muscle glycogenolysis, fat lipolysis, β3)
    8 Stimulation of heart rate & contractility during normal exercise (β1)
  • Vasodilatation of coronary and skeletal muscle arteries (β2)
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11
Q

describe the adrenaline vs noradrenaline effect on resistance vessels

A

b1 on the heart increases rate and force of contraction - adenylate cyclase to cAMP
α2 inhibits adenylate cyclase, reduces Ca2+, and inhibits release of noradrenaline from varicosity. - phospholipase C

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12
Q

describe the angiotensin-aldosterone system (RAAS)

A
  • body’s way of raising blood pressure and maintaining fluid balance.
    *kidneys detect low Na levels and release renin
  • renin converts angiotensinogen into angiotensinogen 1
  • in the lungs enzyme called ACE converted angiotensinogen 1 to angiotensinogen 2
  • narrows blood vessels and stimulates renal glands to release aldosterone
  • Aldosterone tells the kidneys to retain sodium and water while excreting potassium.
  • More water in the blood = higher blood volume and higher blood pressure.
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13
Q

describe vasopressin (ADH)

A
  • hormone that helps the body control water balance and maintain blood pressure.
  • Produced by the Brain
  • Vasopressin is made in the hypothalamus (a part of the brain) and stored in the pituitary gland.
    Triggered by Low Blood Pressure or Dehydration
  • When the body is dehydrated (not enough water) or if blood pressure drops, the brain signals the pituitary to release vasopressin.
  • Water Retention: It acts on the kidneys, making them retain water and reduce urine output, helping to increase blood volume and prevent dehydration.
    Vasoconstriction: It can also cause blood vessels to constrict, which helps raise blood pressure.
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14
Q

describe atrial natriuretic peptide (ANP)

A
  • hormone released by the heart to help lower blood pressure and reduce blood volume.
  • Heart Detects Too Much Blood Volume
    *When the atria (upper heart chambers) stretch due to high blood pressure or too much fluid, special heart cells release ANP.
    *ANP Causes Vasodilation
    *ANP binds to receptors on blood vessel walls.
    This activates cGMP, which relaxes vascular smooth muscle, causing vasodilation (widening of blood vessels).
    *This lowers blood pressure.
    *Opposes Other Systems That Raise Blood Pressure

*Blocks noradrenaline (which normally causes vasoconstriction).
*Inhibits RAAS (reduces renin, angiotensin, and aldosterone levels).
Reduces ADH (vasopressin) → leads to more water loss in urine.

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