Blood Pressure (BP) Regulation Mechanisms


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, Aldosterone → Pressure diuresis
- RAAS
- Renal control of blood pressure and blood volume
- Infinite gain:
- 100% correction of BP/volume to normal
- Gain = Correction / 0 = Infinity.
- 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) | ㅤ |
Vasopressin (V1 receptor) | Terlipressin is used in Rx of esophageal varices |
Angiotensin II | ㅤ |
Vasodilators | ↓ BP |
Calcitonin & related peptide (CGRP) | most potent. |
Nitric oxide | • 2nd messenger: cGMP • Used in Rx of angina. |
Bradykinin | ㅤ |
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 Overactivity → Pulmonary artery hypertension
- Rx: Bosentan (Endothelin blocker)
Natriuretic peptide
- Messenger: cGMP.
- Types of Natriuretic Peptides
Type | Site | Analogue |
A type (ANP) | Atrium | ㅤ |
B type (BNP) | Ventricles | Nesiritide |
C type (CNP) | Vascular endothelium | ㅤ |
- 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 | ㅤ | ㅤ |
↑ 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):


- 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:
- ↓ BP (Baroreflex inhibited)
- Sympathetic Nervous System (+) → Release of norepinephrine →
- ↑ 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
ㅤ | Activated during |
Type A | Atrial systole |
Type B | Atrial diastole |
Chemoreceptor Reflex:

- Second line for BP control.

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
- ↓ PO₂
- O₂-sensitive K⁺ channels close
- Depolarization
- Ca²⁺ channels open
- Ca²⁺ influx
- Dopamine exocytosis
- 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)

Fluctuations in Blood Pressure:


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 |
ㅤ | Traube-Hering Waves ↳ Small BP fluctuations (2-4 mmHg) | Sinus Arrhythmia |
Cough and Sneeze
ㅤ | Mechanism |
Cough | Deep inspiration → forced expiration against closed glottis → sudden glottis opening |
Sneeze | Forced expiration against open glottis [Cannot do voluntarily] |
Valsalva Manoeuvre




- Valsalva Manoeuvre
- Forceful expiration against closed glottis
- ↑ Intrathoracic pressure
Intrathoracic Pressure Changes
Phase | ㅤ | 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 |

Types of Blood Vessels
WindKessel Effect:


ㅤ | Williams syndrome | Marfan syndrome |
Mutations | Elastin Mutation | Fibrillin Mutation |
Leads to | Supravalvular aortic stenosis | Dilatation of aortic root ↳ Rupture → Death |
ㅤ | ㅤ |
Supravalvular AS | • Vitamin D toxicity • William syndrome |
Supravalvular PS | • Noonan syndrome |
ㅤ | 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.
ㅤ | 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

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

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)

- Calculates Vessel resistance
- R = 8 x Viscosity x Length / (π x Radius⁴)
ㅤ | 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


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