4. Regulation of Blood pressure Flashcards

1
Q

Blood pressure

A

Hydrostatic pressure in arterial system pushing blood through the capillary beds to organs / tissues.

results from: Co x TPR

  • > Systolic pressure (maximum 90 - 240 mmHg)
  • > Diastolyc pressure (minimum 60 - 140 mmHg)
  • > Pulse pressure (SP - DP)
  • > major cardiovascular variable regulated by body -> arterioles major resistance vessel
  • > closely regulated as too low (brain / other tissues not receive adequate flow) and too high (extra work for heart + risk of vascular damage)

-> blood vessels don’t burst but tend to leak

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2
Q

Haemodynamics

A

Study of how blood flows

  • > variety of factors influence haemodynamics
    - Vessel length (L)
    - vessel radius (R)
    - viscosity of blood (V)

Flow (Q) = Pressure differece (delta p) / Resistance (R)

CO = (mean arterial p (beginning of tube) - central venule p (end of tube)) / TPR

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3
Q

Factor affecting Blood pressure

A

BP = CO xTPR

Regulation of blood pressure is achieved by controlling the determinants of BP:

1.)

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4
Q

Cardiac Output

A

Heart Rate:
-> determined by sino-atrial node, “pacemaker” -> regulated by nervous activity

  • > Parasympathetic stimulation (low temperature)
  • > Sympathetic nerve stimulation (adrenalin - high temperature)

Control:

  • > Stroke volume
  • > amount of blood ejected by ventricle during single beat
  • > difference between end diastolyc + end systolic volumes (EDV (preload, contractility, afterload) - ESV(filling time, venous term))
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5
Q

Systolic pressure

A
  • > influenced by stroke volume which is th eamount of blood ejected from heart per heart beat
  • > Increase in SV increases pressure, therefore increasing pulse pressure
  • > left ventricular ejection velocity
  • > loss of arterial compliance, e.g. increase stiffness, increases pressure ->
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6
Q

Diastolic pressure

A

-> increase in HR and decrease in pulse pressure

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7
Q

Total peripheral resistance

A

Primary resistance in arterioles -> important in regulating blood pressure

Affected by:

  • > radius of arterioles
  • > vasolidation increase radius - resistance falls
  • > vasoconstriction reduces radius - resistance increases
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8
Q

A - Vascular Tone

A

constriction or tone of blood vessels alter resistance + pressure (hypertension)

Modulated by the action of vasoconstrictors and vasodilators

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9
Q

Vasodilators

A

-> endothelial cells determine dilation + constriction

  • > Sheer stress : Ca 2+ ions released due to the stress -> enzyme Nitric oxide centase released (nitric oxide - very small enzyme and can go from one cell to another very quickly - doesn’t care about obstacles but not very stable hence it can’t affect much in the body, just the neighbouring cells)
  • > nitric oxide activates + releases G cyclase -> G cyclase a signalling molecules, activating GTP -> cGMP, activating PHG -> cannot contract and hence relaxation occurs
  • > G protein has a receptor but activates ATP -> cAMP -> RKA -> Relaxation
  • > Vasodilators such as Bradykinins or ADP can have a bigger impact by releasing Ca 2+
  • > EDF recognise hypertension (high BP) -> relaxation

=> Nitric oxide synthesised by nitric oxide syntahse (NOS) from L-arganine + oxygen

  - > eNOS in endothelium (constitutive)
  - > iNOS induced in monocytes in response to inflammation
  - > nNOS in neurons

=> Peptide hormones: reduce BP

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10
Q

Vasoconstrictos

A

e.g. angiotensin II, thrombin -> all have own receptors (Endothelin, TX A2, PG H2 -> molecules released) -> picked up y smooth muscle cells -> Ca 2+ influx -> constriction

Superoxide another molecule -> present in free radicals -> 1.) gets rid of nitric oxide produced by endothalial cells

=> Endothelin 1 is 21 amino acid peptide released by EC
=> Prostaglanding A2 + H2 released from platelets + EC
=> Superoxide radicals react with NO

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11
Q

Blood flow, pressure + Viscosity

A
  • > blood flow related to pressure
  • > blood viscosity -> dependent on amount of colloidal (non-soluble) material in blood, e.g. lipoproteins, RBC alter viscosity
  • > volume fraction of colloidal material increases viscosity

=> colloidal partical such as lipoproteins are in suspension due to attractive + repulsive van der waals + electrostatic forces -> there is a balance - come together and don’t go further away from each other
=> alteration in electrolytes can neutralise these charges allowing the
=> Oxidation neutralises the charge of the surface of these particles -> e.g. smoking oxidises lipoproteins -> allows them to come together easier -> remember: Lana

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12
Q

Aggragation of lipoproteins

A
  • > separated -> 4 times the volume (vol. fraction)
  • > aggregation: stuck together -> volume fraction 4 + all the dead volume between them -> increased volume fraction hugely
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13
Q

Blood Volume

A
  • > decrease in blood volume -> loss of blood, e.g. haemorrhage / chronic bleeding
    - > dehydration + fall in CO
  • > Increase in Blood volume
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14
Q

Neuronal regulation of BP

A
  • > major cardiovascular control centre in in medulla of brain
  • > VASOMETER CENTRE one of the subgroups within control centre -> consists of group of
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15
Q

Baroreceptors

A
  • > pressure sensors
  • > located in walls of large arteries in neck and thoracic regions
  • > rapid response system for dealing with change in BP
  • > Stimulated by stretch of arterial walls caused by rise in BP
  • >
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16
Q

Chemoreceptors

A
  • > Located in carotid + aortic bodies

- > respond to increased H+, increased CO2 + most strongly to hypoxia (low O2 tension)

17
Q

SUMMARY

A
  • > regulation of BP depends on control of CO + TPR
    • control of CO depends on regulation of HR + SV
    • TPR determined by degree of arteriolar vasoconstriction