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Physiology- CP > Vascular Control > Flashcards

Vascular Control Flashcards

1
Q

What is the equation for flow?

A

Flow = Pressure difference/ resistnace

  • Resistance generated in small arteries
  • R = 1/radius
  • Small changes in diameter can largely and temporarily change blood flow in a vessel
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2
Q

Which organs have the highest oxygen consumption?

A
  • Liver and GI
  • Kidney much lower than distribution(filtration)
  • Skeletal muscle- increases with exercise
  • Heart uses more than blood supply suggests
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3
Q

What is the equation for tissue perfusion?

A
  • Perfusion = pressure gradient/resistance
  • Flow takes path of least resistance
  • R - 1/r^4
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4
Q

What is the equation for total resistance in the system with parallel vascular beds?

A
  • Total resistance in system = 1/resistance of any given arterial bed
  • Each tissue can regulate its own resistance
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5
Q

Describe how exercise effects blood flow to parallel vascular beds

A
  • HR and SV increases
  • Amount of blood going to tissues increases
  • Regional control is needed- because every vascular bed in every tissue behave the same way
  • This is why individual beds are self-regulatory
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6
Q

Describe smooth muscle contraction

A
  • Depolarisation of membrane and opening of voltage gated Ca channels
  • Ca influx and Ca induced Ca release from intracellular stores
  • Contraction via MLCK activation
  • Overlapping of myosin filaments and constriction
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7
Q

Describe activation in smooth muscle

A
  • Agonist-induced increase in Ca through opening of ligand-gated Ca channel or inositol triphosphate
  • Diacyl glycerol release of Ca from stores
  • No changes in membrane potential
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8
Q

Describe Level 1 intrinsic control

A
  • Mechanical stimuli- myogenic stretch and shear response

- Response of artery to physical force that acts upon them ,autoregulation

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9
Q

Describe Level 2 Intrinsic control

A
  • Local mediators released via cells in vicinity that affect what vascular smooth muscle is doing
  • Either constricts/dilates underlying smooth muscle
  • Endothelial regulation + other metabolites and autacoids in response to local demands
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10
Q

Describe level 3 extrinsic control

A
  • Systemic regulation (nerve and hormones)

- Sympathetic activation constricts arteries

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11
Q

What parts of the body are primarily intrinsic?

A
  • Brain, kidney and heart
  • Local control regulating flow
  • Not extremely influenced by what happens globally
  • Global change has limited impact on what is happening in brain/heart
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12
Q

Is the skin intrinsic or extrinsic and why?

A
  • Primarily extrinsic
  • Blood flow to skin about thermal regulation
  • If one is cold, blood flow to skin decreased
  • Cool peripheries consequence of low pressure
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13
Q

Is skeletal muscle intrinsic or extrinsic?

A
  • Primarily extrinsic at rest

- During exercise, local metabolites tend to dominate (more local)

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14
Q

Describe the myogenic response of smooth muscle

A
  • Stretch–> contraction
  • Exact mechanism unknown- involves increase in intracellular stores
  • Seen in many vascular beds (cerebral, renal etc.)
  • Arteries always slightly constricted- basal tone, can be in/decreased, stabilises flow and prevents excessive perfusion
  • Important in auto-regulation
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15
Q

What are the roles of vascular endothelium?

A
  • Interface btwn blood and body tissues
  • Controls blood coagulation
  • Regulated vascular structure
  • Mediated inflam responses
  • Regulates vascular tone
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16
Q

What mediators does vascular endothelium release?

A
  • Nitric oxide
  • Endothelins
  • Prostaglandins (PGE2, PGI2)- platelet aggregation
17
Q

What is NO and how is it produced?

A
  • NO produced by NO synthase
  • Forms eNOS + nNOS constantly produce NO
  • inducible iNOS in smooth muscle and macrophages
  • NO- vasodilator released by shear stress and ACH and bradykinin
  • Anti-thrombogenic/atherogenic
18
Q

Describe the NO pathway

A
  • Receptor bind- Ca influx, phosphorylation of eNOS
  • Arginine–> citrulline + NO
  • Diffuses into lumen preventing platelet aggregation
  • Also diffuses down to smooth muscle- activates guanylate cyclase
  • Production of cyclic GMP
19
Q

What disruptions are there to NO pathway?

A
  • Loss of eNOS/Arginine- no NO produced- thrombogenic surface
  • Damage of endothelium, reduces NO capacity, increased resistance and generation of a thrombogenic surface
20
Q

What drugs interact with NO pathway?

A
  • Nitrates, e.g. GTN in angina- act as NO is released via metabolism
  • Phosphodiesterase inhibitors (t5), e.g. sildenafil (Viagra) for ED and pulmonary HT, prevents breakdown of cyclic GMP
21
Q

What other endothelial pathways are there (other than NO)?

A
  • Prostaglandins- NSAIDS, arachidonic acid metabolites
    • Prostacyclin, PGI2, PGE2- act of adenylate cyclase- cAMP
  • Endothelial-derived hyperpolarise factos hyperpolarise smooth muscle causing relaxation
    • important in microvasculature
    • K influx
22
Q

What can endothelial damage lead to?

A
  • Atherosclerosis and hypercholesterolaemia
  • Diabetes and metabolic syndrome
  • Smoking
  • Hypertension/ preeclampsia
  • Ageing and menopause
  • Less relaxation and more platelet aggregation
23
Q

Describe metabolites in vascular control

A
  • Number of waste products- some vasoactive
  • Increased CO2, K, H+ and adenosine and O2 promote vasodilation
  • Acidity- dilates muscle
  • Adenosine- go up when O2 levels fall and insufficient ATP made- drives relaxation of vascular system-> promotes dilation and perfusion
  • Increased oxygen consumption and metabolism decreases resistance and drives increased perfusion
24
Q

What is metabolic hyperaemia?

A
  • Increased metabolic rate in tissue- increases O2 turnover
  • Accumulation of metabolites- CO2, H+, K+, adenosine
  • All O2 consumption will produce more CO2- acidity
  • Local vasodilation, lowered resistance increases flow
  • Accumulated metabolites flushed out
  • Appropriate blood flow to match metabolic rate
25
Q

What other autocoids are there?

A
  • Produced by many cells- local action
  • Released by cells near vessels- immediate impact
  • Pathological (e.g. inflammation)
  • E.g. histamine, bradykinin, serotonin, eicosanoids and prostanoids (prostaglandins, thromboxanes, leukotrienes)
  • Mixture of dilators and constrictors
26
Q

Describe extrinsic neuronal/hormonal control

A
  • Vascular system mainly SNS (central control)
    • Increases HR + SV, vasoconstriction via α-1 adrenoceptors
  • PNS less common along with other sensory fibres
    • Very few arteries
  • Number of hormones are also vasoactive- either constrict or dilate vessels
27
Q

Describe vasoconstrictor fibres

A
  • Sympathetic- vascular tone
  • Drive slight constricted level of arteries
  • NA- α-1 adrenoceptors
  • Increased symp activity increases vasoconstriction
  • Symp cholinergic- ACh
  • PNS mediated by ACh and some non- adrenergic/ cholinergic transmitters
  • Nociceptive C-fibres mediated by neuropeptides such as CGRP
  • Not all sympathetics
28
Q

What are huge indicators of sympathetic activation?

A
  • Cold clammy peripheries

- Tachycardic, tachypnoeic

29
Q

Describe vasoactive hormones

A
  • Adr from adrenal medulla
  • Part of sympathetic activation, NA acts at α, and Adr at β
    • Predominantly dilatory
    • Constriction/ dilation is vascular bed dependent
  • Ang II acts on AT receptors potent vasoconstrictor
  • Vasopressin (ADH)- vasoconstrictor
  • Insulin and oestrogens- dilator

Physiology- CP (19 decks)

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