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Life support (Year 1) > CVS: Vascular Tone Regulation > Flashcards

CVS: Vascular Tone Regulation Flashcards

1
Q

What is vascular tone?

A

Degree of constriction of a blood vessel relative to maximum dilation

Controlled by contractile state of vascular smooth muscle cells (VSMCs)

Vascular tone is present in arteries, arterioles and veins, not capillaries as they don’t contain VSMCs.

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2
Q

What does vascular tone control?

A

TPR

TPR is inversely proportional to blood vessel radius

Therefore vascular tone controls blood pressure and blood flow and is a major therapeutic target to treat CVS diseases

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3
Q

Why is vascular tone regulated?

A
  • Intrinsic controls (e.g. role of endothelium, immune cells, platelets, stretch)
    • Regulate local blood flow to organs/tissue (Regional hyperaemia)
  • Extrinsic controls
    • Regulate TPR to control BP
    • Brain function selectivity alters blood flow to organs according to need e.g. During exercise, hypovolemia etc.
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4
Q

How is vascular tone regulated?

A
  • Sympathetic vasodilator nerves
  • Perivascular sensory vasodilator nerves
  • Metabolic dilator factors: Adenosine, K+, H+, secreted by fat cells
  • Sympathetic vasoconstrictor nerves
  • Parasympathetic vasodilator nerves
  • Hormones - Adrenaline, Ang II, ADH, ANP
  • Platelets - TXA2
  • Immune cells - release histamine
  • ET1 - Constrictor
  • NO, K+, PGI2 - Dilators

Hormones act on endothelium

GENERAL FEATURES:
- Constrictor responses: Act directly on VSMCs
- Dilator responses: Act indirectly on VSMCs via endothelium

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5
Q

How do sympathetic nerves regulate vascular tone?

A

Sympathetic nerves control vasoconstriction.

  • Contract arterioles → Produces vascular tone. Maintains arterial BP and blood flow to brain/myocardium
  • Distinc RVLM neurones - sympathetic pathways innervate diff tissues. Switching on vasoconstriction in some vessels, off in others (so produces vasodilation)
  • Produce pro-capillary vasoconstriction to increase interstitial fluid reabsorption - Reduce capillary pressure, Increase reabsorption due to increase influence of oncotic pressure, support maintenance of blood volume
  • Produces venoconstriction to increase venous return - Venoconstriction → Increase venous return to heart, increase SV via Starling’s law
  • Rostal ventral lateral medulla (RVLM) receives info from other areas brain (e.g. hypothalamus - Central control of BP and blood flow)
  • Preganglionic fibre originates from thoracic spinal cord intermediolateral (IML)
    • In case of adrenal medulla, preganglionic synapses directly with the adrenal medulla, there’s no postganglionic fibre
  • Sympathetic nerve activity is tonic (fires about 1 AP/s). Contributes to vascular tone
  • Fall in sympathetic activity produces vasodilation
  • Post synaptic membrane:
    • Alpha 1 - contraction
    • Alpha 2 - contraction
    • Beta 2 - relaxation
  • Pre synaptic membrane
    • AT1 - increase release of NA (hence RAAS increases sympathetic activity)
    • Alpha 2 - reduce release of NA
    • Local metabolites (K+/adenosine etc.) - reduce release of NA - vasodilation
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6
Q

How do parasympathetic nerves regulate vascular tone?

A

Salivary glands - release Ach/VIP

Pancreas + intestinal mucosa - release VIP

Both these tissues need high blood flow to maintain parasympathetic-mediated fluid secretion

Therefore, parasympathetic nerves release Ach/VIP which act on endothelium, causing release of NO which induces vasodilation

Male genitalia (erectile tissue) - release NO

Release of NO by parasympathetic nerves causes production of cGMP which leads to vasodilation

Sildenagil (Viagra) enhances this effect of NO by reducing metabolism of cGMP by blocking phosphodiesterase 5

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7
Q

How do sympathetic vasodilator nerves produce vasodilation?

A

Some sympathetic nerves produce vasodilation e.g. skin (sudomotor fibres) - release Ach, VIP

Vasodilation associated with sympathetic-mediated sweating

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8
Q

How do nociceptor vasodilator fibres regulate vascular tone?

A

Stimulation of sensory C-fibre (nociceptors) nerves by trauma, infection etc,:

  • Release Sub P, cGRP
    • Act on mast cells to release histamine
    • Act on endothelium and VSM
    • Both produce vasodilation called ‘flare’ in skin
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9
Q

What are functions of the endothelium?

A
  • Vascular tone
    • Production of NO and prostacyclins (PGI2)
    • Vasodilation, balance of vasoconstriction action of sympathetic nerves
  • Blood-tissue interactions
  • Production of Ang II, endothelium surface contains ACE
  • Blood clotting, inflammatory pathway, angiogenesis, atheroma

Breakdown of endothelium function - termed endothelium dysfunction e.g. by hypertension, diabetes, cigarette smoking

Reduces NO/PGI2 production, enhances vascular tone (vasoconstriction). Shift balance to sympathetic activity

Hence, endothelium dysfunction’s linked to CVS diseases

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10
Q

Describe endothelium-mediated vasodilation

A

NO:

  • Blood flow detected by receptors, (through shear stress) → Constant release of NO
  • This activates eNOS (endothelium nitric oxide synthase) which produces NO
  • NO is lipophilic, soluble, freely diffusible and stimulates guanylate cyclase (GC)
  • NO diffuses through endothelial cell, activates GC which activates cGMP cycle, converts GMP -> cGMP -> PKG, and this induces vasodilation
  • Vascular tone control by tonic sympathetic activity (constriction) + tonic NO release (dilation)

PGI2:

  • Blood flow detected by receptors to induce Shear stress response, inflammatory factors, Ach (Sub P, histamine, bradykinin, Ach, VIP)
  • Membrane lipids into PGI2 via cyclooxygenase (COX)
  • PGI2 acts on prostanoid receptor (Gs → AC→ cAMP → PKA pathways, induces vasodilation)
  • Tonic PGI2 production’s important in maintaining blood flow in renal arterioles
  • Needed to maintain glomerular filtration rate (GFR) and kidney function
  • COX inhibition (NSAIDs), reducing PGI2 is potentially dangerous in kidney failure
  • Important pathway in inflammation-mediated vasodilation
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11
Q

Why do PKG and PKA produce vasodilation?

A
  • Increase Ca ATPase (SERCA) - Increase uptake into SR and exclusion from cell
  • Increase K+ channel activity → hyperpolarisation → decrease VgCCs
  • Decrease MLCK

All of these actions reduce Ca2+ levels, therefore reducing action of contractile mechanisms in smooth muscle

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12
Q

Describe the role of adrenaline in controlling vascular tone

A
  • Released due to sympathetic nerve stimulation
  • Mainly from adrenal glands
  • Acts on alpha-1 adrenoceptors on VSMCs
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13
Q

Describe the role of Ang II in controlling vascular tone

A
  • Formed from RAAS
  • Very potent vasoconstrictor
  • Acts on AT1 receptors on VSMCs
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14
Q

Describe the role of ADH in controlling vascular tone

A
  • Released from posterior pituitary gland
  • Acts on V1-receptors on VSMCs
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15
Q

When are adrenaline, ang II and ADH released?

A

When there’s a decrease in blood pressure due to a decrease in blood volume/TPR

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16
Q

Describe the role of endothelin-1 (ET1) in controlling vascular tone

A
  • Released from endothelium
  • Acts on ETa receptors on VSMCs
17
Q

Describe the role of thromboxane (TXA2) in controlling vascular tone

A
  • Released from aggregating platelets
  • Acts on TP receptors on VSMCs
  • Important vasoconstrictor alongside clotting process
18
Q

How do vasoconstrictors increase vascular tone?

A

They activate same Gq-protein-coupled pathway in VSMCs

  • Receptors activates (alpha 1, Ang II, AT1, ET-1) - Induces conversion of PIP2 into DAG and IP3
  • IP3 binds to IP3 receptors on SR, increases Ca2+
  • DAG increases membrane excitability - leads to depolarisation
  • Activation of VGCa channels increases Ca2+ influx.
  • Increase Ca = Increase Ca2+/calmodulin complex, increased MLCK activation, increases contraction
19
Q

Describe the role of ANP in controlling vascular tone

A

ANP - vasodilator

  • Released by specialised atria myocytes
  • Secreted by increased filling pressures which stimulate stretch receptors
  • Act at NP receptors on vascular smooth muscle (activate cGMP pathway in VSMCs like nitric oxide)

Reduces BP by:

  • Systemic vasodilation - opposes action of Na, adrenaline, Ang II, ADH, ET-1, TXA2
  • Dilation of renal afferent arteriole - Increases glomerular filtration rate and increases Na+ and H2O excretion by kidney - Reduces blood volume

Decreases release and actions of aldosterone, renin, ADH

20
Q

How does stimulation of B2 adrenoceptors on VSMC produce vasodilation in coronary and skeletal muscle arterioles?

A
  • B2 adrenoceptor stimulation → PKA activity
  • Increases SERCA (Ca2+ ATPase) - Increase uptake into SR/exclusion from cell
  • Increases K+ channel activity → Hyperpolarisation → decreases VgCa channels
  • Decreases MLCK

This helps increase blood flow to heart and skeletal muscle during exercise

21
Q

In what conditions may vasoconstriction increase?

A
  • Hypoveolemia - Decrease in blood volume e.g. haemorrhage, dehydration, decreases SV/CO, decreases BP
  • Sepsis - Systemic infection, excessive systemic vasodilation, decreases TPR, large drop in BP, no drive for end organ perfusion, end organ damage
  • Anaphylaxis - Hypersensitivity reaction, systemic vasodilation, poor end organ perfusion
  • Heart failure - Poor CO, poor BP, poor end organ perfusion

In these conditions, vasoconstriction must be induced to increase vascular tone/TPR and raise BP to normal to maintain correct end organ perfusion

22
Q

When are NORAD, adrenaline and ADH used to increase vasoconstriction?

A
  • NORAD has higher affinity for alpha than beta adrenoceptors, whereas adrenaline is the opposite
  • NORAD is given primarily to act at alpha-1 receptors on VSMCs to increase TPR and BP, without having significant actions on heart (B1) - cardiac protective, doesn’t make heart work harder to increase BP, blood flow. This is important in conditions such as sepsis, which can cause severe heart failure
  • Adrenaline is given in high concentrations to have an action on both B1 on heart and alpha 1 on VSMCs to raise BP (also Beta-2 in lungs to give bronchodilation), e.g. epipen for anaphylaxis
  • ADH - Can be given in sepsis
23
Q

Why may vasodilation need to be increased?

A

Hypertension → Increases afterload, which can cause poor CO and increases work done by heart.

24
Q

Describe vasodilator drug targets

A
  • Block Gq receptors (ARB, ACEi, alpha-1/ETa inhibitors) - Prevent vasoconstriction pathway
  • Prevent increases in membrane excitability (nitrates, K channel openers) - Hyperpolarisation, inhibit VGCa channels
  • Block VGCa channels (Dihydropyridines- CCBs) - Decrease Ca2+ influx
  • Nitrates (GTN) - Increases exclusion of Ca2+ out of cell and uptake into SR. Also decreases action of MLCK

Life support (Year 1) (26 decks)

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