Blood Pressure Regulation Mechanisms, Types of Blood Vessels😍

Blood Pressure (BP) Regulation Mechanisms

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Speed of Action:

Short term/Rapid (seconds-minutes):

  • Baroreceptor > Chemoreceptor > CNS Ischemic Response.

Intermediate (minutes-hours):

  • Renin - Angiotensin II (vasoconstriction)
  • Capillary fluid shift
  • Stress relaxation

Long-term (hours-days):

  • ADH, ANP, AldosteronePressure diuresis
  • RAAS
  • Renal control of blood pressure and blood volume
    • Infinite gain:
      • 100% correction of BP/volume to normal
      • Gain = Correction / 0Infinity.
      • NO RESIDUAL ERROR
      • Slow system, takes time

Potency:

  • RAAS >>
  • CNS Ischemic Response
    • Last Ditch Response

Chemical Regulation of BP

Vasoconstrictors
↑ BP
Urotensin 
most potent
Norepinephrine 
α agonist
Endothelin (ET)
Vasopressin (V1 receptor)
Terlipressin is used in Rx of esophageal varices
Angiotensin II
Vasodilators
↓ BP
Calcitonin & related peptide (CGRP)
most potent.
Nitric oxide 
• 2nd messenger: cGMP
• Used in
Rx of angina.
Bradykinin
Natriuretic peptide
Messenger: cGMP
BNP Analogue: Nesiritide
Endothelin
• Overactivity cause PAH
• Rx: 
Bosentan (Endothelin blocker)

Endothelin (ET):

  • Produced from endothelial cells of lungs
  • Binds to ETA receptor and ETB receptor
  • Endothelin OveractivityPulmonary artery hypertension
  • Rx: Bosentan (Endothelin blocker)

Natriuretic peptide

  • Messenger: cGMP.
  • Types of Natriuretic Peptides
    • Type
      Site
      Analogue
      A type (ANP)
      Atrium
      B type (BNP)
      Ventricles
      Nesiritide
      C type (CNP)
      Vascular endothelium
  • Site of Action
    • Terminal DCT and CD.
  • Actions
    • Action
      Key Point
      Mechanism / Effect
      1
      Natriuresis
      Afferent arteriole dilation → ↑ GFR → ↑ Na⁺ excretion
      2
      Physiological Antagonism With RAAS
      ↑ Na⁺ → ANP activated;
      ↓ Na⁺ → RAAS activated
      Regulation
      ↑ ANP
      Fluid overload
      Stretch of atria↑ ANP release
      ↓ ANP
      Hypovolemia
      Reduced atrial stretch↓ ANP release

Baroreceptor Reflex: Marey's Law

  • Mnemonic:
    • Marey → high BP
    • Bp kudiyapo (↑↑BP) Baril (Baroreceptor) Poi
    • Nattampidich (NTS) vannu
    • Sis (CIC) Para (Parasympathetic) vachu
    • Amma Kavalam (CVLM) nokki adichu → “Veedu Mudipikkathe” (VMC) Roadilirakki Vittu (RVLM)
  • First line to regulate BP.
  • Negative Feedback system.
  • Activation: Increase in blood pressure (stretch).
  • Normal baroreceptor gain- 2.
    • Correction is opposite to disturbance

Marey's Law:

  • ↑ BP leads to reflex ↓ HR 
    • BP x HR = constant
  • Sister (CIC) Mary () → Para

Baroreceptors

  • Carotid sinus:
    • Small dilations in internal carotid artery.
    • Afferent nerve: CN 9 (Hering nerve).
  • Aortic arch:
    • Wall of aorta
    • Afferent nerve: CN 10 (Cyon's nerve).

Most Sensitive Stimulus: 

  • Distension
    • ↑↑ Pulse pressure > ↑↑ MAP
    • 70 - 140 
  • Response: 
    • Up to MAP of 180 

Centre (Nucleus Tractus Solitarius in medulla):

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  • BP =
    • Pulse pressure >> MAP

Clinical Aspects:

  • Occlusion of common Carotid artery:
    • ↓ Blood flow to internal carotid artery → ↓ Pressure
    • Baroreflex inhibited → ↑ BP & ↑ HR (↑ Sympathetic activation).
  • Clamping above carotid sinus:
    • ↑ Pressure
    • Baroreflex activated → ↓BP & ↓HR (↑ Sympathetic inhibition).
  • Supine → On Standing immediately
    • If SNS underactivity → Fall due to postural hypotension.
    • Normal:
        1. ↓ BP (Baroreflex inhibited)
        1. Sympathetic Nervous System (+) → Release of norepinephrine
        1. ↑ HR, Vasoconstriction (via α-receptors) → ↑ Total peripheral resistance.
  • Impact of Lying Down
    • Lying down → ↑ Venous return → Stored in Pulmonary veins → Pulmonary congestion → Breathlessness (Orthopnea)
  • Carotid Sinus Massaging/ Czermak Hering Test:
    • Activates PNS →Vagus → Ach release → M2 receptors
    • Baroreflex ↓HR.
    • Used in treatment of PSVT
    • Mark gave her ring → carotid kiss

Other Baroreceptors:

  • Atrial & Pulmonary artery baroreceptors
    • Low pressure receptor (volume sensing receptor).

2 Types of atrial stretch receptors

Activated during
Type A
Atrial systole
Type B
Atrial diastole

Chemoreceptor Reflex:

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  • Second line for BP control.

Cause of fetal heart acceleration

  • Carotid body chemoreceptors > Autonomic Brainstem regulation
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Location

  • Carotid bodies: At carotid bifurcation
  • Aortic bodies: Near arch of aorta (usually >2)
  • Actual chemoreceptors:
    • Type I Glomus cells
  • Type II: Glia-like supporting cells

Mechanism

  • Glomus cells have oxygen-sensitive K⁺ channels

Stimulated by (in arterial blood)

  • ↓ PO₂ (Hypoxia)Primary/Direct stimulus
  • ↑ PCO₂ (Hypercapnea) → Most sensitive
  • ↑ H⁺ (Acidosis)
  • Hypotension
  • Most potent stimulus: Cyanide poisoning (histotoxic hypoxia)

MOA – Glomus Cells

  1. ↓ PO₂
  1. O₂-sensitive K⁺ channels close
  1. Depolarization
  1. Ca²⁺ channels open
  1. Ca²⁺ influx
  1. Dopamine exocytosis
  1. Stimulates respiratory centre
  • Afferents, Center, Efferents: Same as Baroreceptors.

Response:

  • Chemoreceptor activation
    • Positive signals to both 
      • Vasomotor Center (RVLM)
        • Strong sympathetic activation → ↑ BP
      • Cardiac Inhibitory Center (CIC)
        • Parasympathetic activation → ↓ HR
          • Mild activation↓HR
          • Severe activation↑HR
            • indirectly via ↑ ventilation

Overall Effect:

  • Always ↑BP

CNS Ischemic Response (CIR):

  • 2nd most Potent.
  • “Last line of control” / "Last Ditch Resort" / "Last Ditch Response"
BP analogues
Formula
Pulse pressure
SBP - DBP
Mean arterial pressure (MAP)
DBP + 1/3 pulse pressure
1/3 SBP + 2/3 DBP
Normal: 93-100 mm Hg
Cerebral Perfusion Pressure
MAP – intracranial pressure

Activation: 

  • Severe ↓↓ in BP
    • < 50 mmHg 
    • CNS hypoxia/ischemia

Response: 

  • Activation of RVLM (SNS)
    • Most powerful response
    • Massive sympathetic activation
    • Increase MAP (≥ 250 mmHg)
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Fluctuations in Blood Pressure:

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Progressive blood loss

  • Mayer waves/vasomotor waves:
    • Slow, rhythmic BP fluctuations
    • Due to interplay of Baro/Chemo/CIR.
    • Interval:
      • 26s (animals)
      • 7-10s (humans)
Fluctuation with respiration
of BP
of HR
Inspiration
Transient ↓BP
↑HR
Expiration
Transient ↑BP
↓HR
Traube-Hering Waves
Small BP fluctuations (2-4 mmHg)
Sinus Arrhythmia

Cough and Sneeze

Mechanism
Cough
Deep inspirationforced expiration against closed glottissudden glottis opening
Sneeze
Forced expiration against open glottis
[Cannot do voluntarily]

Valsalva Manoeuvre

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  • Valsalva Manoeuvre
    • Forceful expiration against closed glottis
    • ↑ Intrathoracic pressure

Intrathoracic Pressure Changes

Phase
Mechanism
Result
1
Onset of Strain
Compression of pulmonary and aortic arteries
Rapid ↑ BP
2
Continued Strain
Maintained Venacava compression
↳ ↓ venous return
Causes ↓ BP
3
Release of Strain
Blood pooling in dilated pulmonary capillaries
Further ↓ BP 
4
Recovery
Surge in venous return
Overshoot in BP
• Then normalization
Phase 4
Phase 4

Types of Blood Vessels

WindKessel Effect:

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Williams syndrome
Marfan syndrome
Mutations
Elastin Mutation
Fibrillin Mutation
Leads to
Supravalvular aortic stenosis
Dilatation of aortic root
↳ Rupture → Death
Supravalvular AS
Vitamin D toxicity
William syndrome
Supravalvular PS
Noonan syndrome
Seen in
GNAS
Mccune Albright
Cardiac Myxoma
GNAS 1
• Pseudohypoparathyroid/ Albright Hereditary Osteodystrophy
GNAQ
Sturge Weber (Sporadic)
  • Elastic property of large arteries → Allows vessels to distend during systole → Stores energy during systole → Releases energy as kinetic energy during diastole → Helps push blood to the periphery.
Vessels
Functions
Conduit Vessels
Large arteries
Conduct blood
Resistance Vessels
Arterioles
Control blood distribution
Exchange Vessels
Capillaries
Substance exchange
Capacitance Vessels
Venous System
Store blood
High distensibility and compliance
High volume low pressure system
Shunt Vessels
AV anastomoses
Bypass capillaries (fingertips, earlobes)
Temperature regulation
• No exchange of substances

Vena Cava

  • Has max diameter
  • Exhibits minimum BP

William Syndrome

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  • Chromosome 7 micromutation
  • Elastin Mutation
    • Results in Williams syndrome
  • Overfriendly
  • HyperCalcemia
  • Elfian facies
  • Leads to Supravalvular aortic stenosis
    • Differential BP
      • Right arm BP > Left arm Bp > Lower Limb

Williams syndrome
Marfan syndrome
Mutations
Elastin Mutation
Fibrillin Mutation
Leads to
Supravalvular aortic stenosis
Dilatation of aortic root
↳ Rupture → Death
Supravalvular AS
Vitamin D toxicity
William syndrome
Supravalvular PS
Noonan syndrome
Seen in
GNAS
Mccune Albright
Cardiac Myxoma
GNAS 1
• Pseudohypoparathyroid/ Albright Hereditary Osteodystrophy
GNAQ
Sturge Weber (Sporadic)

Types of Blood Flow

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Feature
Laminar flow
Turbulent flow
Pattern
Streamlined
Disordered
Velocity
Highest at center
• Lowest at walls
Velocity in multiple directions
Cell position
Cells in center
Random distribution
Vessel condition
Normal vessels
Compressed / obstructed vessels
Sound
Silent
Noisy
Murmurs, Korotkoff sounds
Reynolds Number (Re)
< 2000: Always laminar
> 3000: Always turbulent

Determined by Reynolds Number (Re)

  • Re = (Density x Diameter x Velocity) / Viscosity
  • Velocity:
    • Most important determinant
    • due to Critical Velocity

Poiseuille's Equation (Hagen-Poiseuille Equation)

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  • Calculates Vessel resistance
  • R = 8 x Viscosity x Length / (π x Radius⁴)
    • Resistance
      Flow
      Directly proportional
      Blood viscosity & vessel length
      Radius (R⁴)
      Inversely proportional
      Radius (R⁴)
      Length of vessel

Poiseuille's Law (Formula for Blood Flow)

  • F = ΔP x r⁴ x π / 8hl
    • F: Rate of blood flow
    • ΔP: Pressure difference between vessel ends
    • r: Radius of the vessel
    • l: Length of the vessel
    • h: Viscosity of the blood

Blood Flow & Oxygen Consumption in Organs

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Maximum and Minimum Values Table

Parameter
Maximum Value
Minimum Value
Percentage of Total Cardiac Output (%)
Liver - 28
Heart - 4.7
Blood Flow (ml/min)
Liver - 1500
Heart - 250
Blood Flow per 100g/min
Kidney - 420
Skeletal Muscle - 2.7
Arteriovenous O₂ Difference (ml/min)
Heart - 114
Kidney - 14
Oxygen Consumption (ml/min)
Liver - 51
Skin - 12
Oxygen Consumption (ml/100g/min)
Heart - 9.7
Skeletal Muscle - 0.2
  • Liver → large organ → so max blood flow, ↑↑ % of total CO
  • Highest O2 consumption/g → Heart
  • Highest rate of blood flow/g → Kidney