Nervous and Hormonal Control of Vascular Tone Flashcards Preview

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What are the two types of vascular control (including examples of each)?

    • myogenic response
    • paracrine and autoregulation agents (NO, PGs, Endothelin, K+, H+)
    • physical factors (temperature, shear stress)
    • parasympathetic, sympathetic sensory vasodilator nerves
    • sympathetic vasoconstrictor nerves
    • Adrenaline, Angiotensin II, Vasopressin, Atrial natriuretic peptide

Paracrine signaling meaning - It is a form of cell-to-cell communication in which a cell produces a signal to induce changes in nearby cells, altering the behavior of those cells


What are the roles of intrinsic and extrinsic control?

  • INTRINSIC CONTROL: - regulates local blood flow to organs/tissues [E.g. regional hyperaemia (an excess of blood in the vessels supplying an organ or other part of the body)].
  • EXTRINSIC CONTROL: - regulates TPR of the entire system to control blood pressure.
    • Brain function selectivity alters blood flow to organs according to need (eg. during exercise, thermoregulation, etc.)
      • NERVES (vasoconstrictors, such as noradrenaline, and vasodilators, such as acetylcholine and NO)
      • HORMONES (vasoconstrictors, such as adrenaline, angiotensin II, vasopressin, and vasodilators, such as atrial-natriuretic peptide (ANP))


Describe the mechanism of the most widespread and important extrinsic control.

  • The most important and widespread extrinsic control is the sympathetic vasoconstrictor system.
  • TPR controlled by vascular tone- constant sympathetic nervous system affect in arteriole, sending noradrenaline to vessels to make vessels constrict. Also nitric oxide produced by endothelial cells makes vessels dilate. Therefore there is a balance in dilation and constriction, so when something happens, we can vary blood flow.
  1. The Rostral Ventrolateral Medulla (RVLM) of the brain recieves information from the Caudal Ventrolateral Medulla (CVLM).
  2. It then sends a signal down the main excitatory drive to the thoracic (T1-L2) spinal cord.
  3. This goes through the intermediolateral cell column (IML) of the spinal neurones, with contain pre-ganglionic sympathetic neurones.
  4. It then sends a signal down the sympathetic fibres to release noradrenaline on the β2 receptors for vasoconstriction.
  5. This increases the BP and SV in the heart. It also sends signals down to the adrenal medulla to release adrenaline, which causes α1 constriction (but β2 relaxation).


Describe how sympathetic innervation of the arterioles leads to release of NA, and what becomes of it.

  1. An action potential moves down the axon and arrives at a varicosity (A varicosity innervates the adventitia, the outermost layer of a blood vessel wall).
  2. Depolarisation occurs at the varicosity, activating voltage-gated Ca2+ channels.
  3. An influx of Ca2+ causes the release of neurotransmitters, mainly noradrenaline.
  4. The noradrenaline diffuses to the vascular smooth muscle where it mainly binds to α1, causing constriction. It will also bind to some α2, causing constriction, and β2, causing relaxation. There is a modulation of responses in both constriction and dilation.
  5. The noradrenaline is then taken up again, and either recycled or broken down.
  • Adrenaline from the adrenal glands that is released into the blood circulation can also act as α1 or β2 receptors.


Describe what happens at the varicosity in detail.

  1. Depolarisation by the action potential opens VGCC. Ca2+ rushes in. Noradrenaline (in vesicles) is released due to Ca2+.
  2. There is some negative feedback because NA can bind to its own α-2 receptor and close the channels and reduce the effect- limits NA release
  3. Metabolites / inflammatory mediators can bind to its own receptors on the varicosity and inhibit the release of NA causing vasodilation to maintain blood flow. Examples include: K+, adenosine, Prostaglandin E1 (PGE1), histamine, serotonin etc
  4. Angiotensin II is a hormone produced in response to change in BP and acts on AT1 receptor to increase NA release and cause vasoconstriction and a rise in BP.
  • Modulation at the neurotransmitter level at the varicosity.


What are some important points about sympathetic vasoconstrictor nerves?

  • They are controlled by the brain stem (RVLM, CVLM. It provides control of blood flow/ blood pressure).
  • It innervates most of the arterioles and veins of the body - sympathetic nerve activity is tonic; tonic sympathetic activity sets vascular tone - a decrease in sympathetic activity producing vasodilation is an important principle in pharmacological treatment of cardiovascular disease.


What are the main roles of the sympathetic vasoconstrictor nerves (with cardiovascular parameters)?

  1. Contract resistance arterioles
    • Produces vascular tone (resistance), allow vasodilation / increased blood flow to occur, controls TPR
  2. Distinct RVLM neurones-sympathetic pathways innervate different tissues
    • Able to constrict some vessels and not others when needed e.g. in exercise, increased sympathetic nerves stimulation to GI (less blood flow), reduce sympathetic nerve stimulation to skin (more blood flow - cool down)
  3. Precapillary vasoconstriction
    • Leads to downstream capillary pressure drop so increased absorption of interstitial fluid into blood plasma to maintain blood volume (important in hypovolemia)
  4. Control TPR
    • Maintains arterial blood pressure and blood flow to brain / myocardium since Pa = CO x TPR
  5. Controls venous blood volume
    • Venoconstriction leads to decreased venous blood volume increasing venous return, this increases SV via Starling’s law.


Describe vasodilator nerves.

  • A few specialised tissues contain vasodilator nerves, as well as vasoconstrictor nerves.
  • Normally, they have a specific function controlling a specific vascular bed rather than global functions.
  • Vasodilation occurs as the vascular tone produced by sympathetic vasoconstrictor nerves is inhibited.
  • There are mainly parasympathetic vasodilator nerves, and a few sympathetic vasodilator nerves and sensory (nociceptive C fibres) vasodilator fibres.


Where are parasympathetic and sympathetic vasodilator nerves found?


  • Salivary gland- release ACh and vasoactive intestinal peptide (VIP)
  • Pancreas & intestinal mucosa- release VIP
    • Both these tissues need high blood flow to maintain fluid secretion. Ach/VIP act on endothelium to release NO and therefore cause vasodilation
  • Male genitalia (erective tissue)- release NO
    • Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilation.
    • Slidenafil (Viagra) enhances this effect of NO by inhibiting the breakdown of cGMP by phosphodiesterase-5.


  • Skin (sudomotor fibres)- 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 coding.
    • Emotional centres in the brain have some control over these fibres, head, face, upper chest- involved in blushing.


Describe the effect of stimulation of sensory (nociceptive C fibres) vasodilator fibres.

  • The stimulation of sensory axon reflex (C-fibres) occurs by trauma, infection, etc.
  • They release a substance called substance P or calcitonin gene-related peptide (CGRP).
  • This acts on mast cells to release histamine.
  • It also acts on the endothelium and vascular smooth muscle.
  • Both the histamine and CGRP produce vasodilation, seen as the 'flare' in the skin.
  • Inflammation is part of the Lewis triple response 1) Local redness 2) Wheal 3) Flare


Name some hormones that affect the control of circulation.

    • adrenaline
    • angiotensin II
    • vasopressin (another name for anti-diuretic hormone, ADH)
    • atrial natriuretic peptide (ANP)
    • insulin
    • oestrogen
    • relaxin


Where do noradrenaline and adrenline work, and what is their effect?

  • In most tissues, such as the GI tract and skin, adrenaline and noradrenaline both cause vasoconstriction.
  • In skeletal muscle and coronary circulation, adrenaline causes vasodilation, while noradrenaline still causes vasoconstriction.
  • In most tissue vasoconstriction due to a1 adrenoceptors
  • Skeletal muscle and coronary arteries have more b2 than a1 adrenoceptors
  • Adrenaline higher affinity for b over a,  mainly acts at b2 to dilate vessels
  • Noradrenaline higher affinity for a, mainly acts at a1 receptors to constrict vessels


Describe the effects of iv adrenaline and iv noradrenaline on common cardiovascular parameters.


Effect on skeletal muscle arteriole (beta-2) causes vasodilation so TPR decreases. Effect on increasing heart rate (beta-1) so CO increases. Not much effect on BP.


TPR increases because of vasoconstriction (alpha 1) so increase in TPR. Sends BP up stimulating baroreceptors and therefore baroreceptor reflex to decrease heart rate. Drop in heart rate causes cardiac output to decrease.


Describe a situation in which the renin-angiotensin-aldosterone system (RAAS) responds to lowered BP.

  1. Starts by a BP drops / dehydration (low NaCl)- detected by kidney.
  2. The kidneys detect stretch, BP and osmotic potential of blood.
  3. Low BP/low osmotic potential makes kidney produce renin.
  4. Renin causes proteolysis (cleaves of 10 amino acids) of angiotensinogen (precursor made in liver) into angiotensin I which goes to lungs where it meets enzyme Angiotensin Converting Enzyme (ACE).
  5. ACE cleaves off two more amino acids from angiotensin I to form angiotensin II.
  6. Angiotensin II goes around the body and causes vasoconstriction, raising TPR and stimulates sympathetic nerves to increase BP.
  7. Angiotensin II also effects brain to increase thirst and increases sympathetic drive on all the vessels.
  8. This increases BP so kidneys can be perfused.
  9. Angiotensin II also acts on adrenal gland on top of the kidneys to produce aldosterone (a steroid) which causes the retention of more Na in order to raise osmotic potential in the blood to allow fluid from interstitial space moves into blood and fluid from kidney follows Na therefore increasing blood volume and therefore blood pressure.


Describe how vasopressin responds to lowered BP.

  • Receptors in aorta (arterial baroreceptors) and left atrium (left atrial receptors) measure stretch and osmotic potential. If they detect dehydration, they will release ADH which increases renal absorption of water
  • The receptors send signal to the nucleus tractus solitarius (NTS) in the brainstem (medulla). NTS sends the signal to caudal ventrolateral medulla (CVLM). CVLM signals hypothalamus to release ADH.
  • If there is a big blood volume and heart is getting stretched and there isn’t much NaCl, (not too dehydrated) - then signal from CVLM is supressed.
    • Therefore stretching of heart, high blood volume- turns off release of ADH
  • Low blood volume = less stretch in baroreceptors. Signal is less so less inhibition of CVLM so increased ADH release.
  • Hypothalamus sends message to posterior pituitary via magnocellular neurons in supraoptic nucleus (SON) and paraventricular nucleus (PVN). Vasopressin (ADH) released and there’s some vasoconstriction to raise BP and antidiuresis (reabsorb more water to increase blood volume).


Describe the mechanism of ANP (atrial natruiretic peptide).

  • Released by specialised atrial myocytes. They are secreted when there is an increased filling pressure which stimulate stretch receptors.
    • Acts at ANP receptors on vascular smooth muscle cells increasing cGMP pathway (like nitric oxide)
    • Systemic vasodilation- opposes action of NA, RAAS and ADH
    • Dilatation of renal afferent arteriole increases GFR. So Na+ and water excretion by the kidney are increased and blood volume goes down decreasing release and/or actions of aldosterone, renin & ADH

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