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    Role of RAAS

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    Jonathan O'Neal
    The renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system play important roles in regulating blood pressure through nervous and humoral mechanisms. RAAS involves the conversion of angiotensinogen to angiotensin I and then angiotensin II, which causes vasoconstriction and sodium retention leading to increased blood pressure. In contrast, the kallikrein-kinin system generates bradykinin which causes vasodilation and lowers blood pressure through mechanisms like stimulating nitric oxide and prostacyclin release from endothelial cells.

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    Role of RAAS

    Uploaded by

    Jonathan O'Neal
    100 views26 pages
    The renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system play important roles in regulating blood pressure through nervous and humoral mechanisms. RAAS involves the conversion of angiotensinogen to angiotensin I and then angiotensin II, which causes vasoconstriction and sodium retention leading to increased blood pressure. In contrast, the kallikrein-kinin system generates bradykinin which causes vasodilation and lowers blood pressure through mechanisms like stimulating nitric oxide and prostacyclin release from endothelial cells.

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    The renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system play important roles in regulating blood pressure through nervous and humoral mechanisms. RAAS involves the conversion of angiotensinogen to angiotensin I and then angiotensin II, which causes vasoconstriction and sodium retention leading to increased blood pressure. In contrast, the kallikrein-kinin system generates bradykinin which causes vasodilation and lowers blood pressure through mechanisms like stimulating nitric oxide and prostacyclin release from endothelial cells.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    100 views26 pages

    Role of RAAS

    Uploaded by

    Jonathan O'Neal
    The renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system play important roles in regulating blood pressure through nervous and humoral mechanisms. RAAS involves the conversion of angiotensinogen to angiotensin I and then angiotensin II, which causes vasoconstriction and sodium retention leading to increased blood pressure. In contrast, the kallikrein-kinin system generates bradykinin which causes vasodilation and lowers blood pressure through mechanisms like stimulating nitric oxide and prostacyclin release from endothelial cells.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
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    of 26

    BLOOD PRESSURE REGULATION

    AND
    ROLE OF RAAS

    BIOPREXUM TRAINING
    First day : 08.00 09.00
    What Is Blood Pressure?

    Blood pressure is the force on the


    walls of the arteries as the blood
    circulates around the body.
    Blood pressure: normal values

    SBP < 120 mmHg


    DBP < 80 mmHg

    JNC VII
    Blood Pressure (BP)

    BP = CO x PR

    Cardiac Output Peripheral


    resistance
    CO = HR x SV
    1. REGULATION OF BLOOD PRESSURE
    Blood pressure regulation

    Immediate Delayed
    regulation
    regulation

    NERVOUS REGULATION HUMORAL REGULATION

    Sympathetic System Hormones


    Parasympathetic System
    Blood pressure regulation :
    NERVOUS

    Blood pressure control by the baroreceptors


    heart, carotid arteries and aorta

    Communication of the information to the SNC

    Nervous counter-regulation
    Blood pressure regulation :
    NERVOUS

    BP BP
    The baroreceptors
    located in the carotid
    sinuses detect changes
    in BP.
    Nervous
    Nervous regulation
    regulation
    Sympathetic
    Sympathetic parasympathetic
    parasympathetic
    stimulation
    stimulation stimulation
    stimulation

    BP BP
    Blood pressure regulation :
    NERVOUS
    Adrenaline Acetylcholine
    Parasympat
    Organ Sympathetic Effects hetic Effects
    receptors receptors
    Heart 1 cholinergic
    HR HR
    SV SV
    excitability excitability
    conductIbility conductibility

    Vesel 1 >> 2 vasoconstriction no no


    Kidney 1 Renin no no

    Lungs bronchodilation cholinergic Broncho


    constriction
    Blood pressure regulation :
    HUMORAL
    BP BP
    Angiotensin II Humoral
    Aldosterone Bradykinin
    Adrenaline
    regulation
    ADH (Antidiuretic
    hormone)

    BP BP
    Blood pressure regulation :
    HUMORAL

    BP origin

    Angiotensin II Plasma (& tissue)


    Aldosterone Adrenal cortex
    Adrenaline Adrenal medulla
    ADH Posterior pituitary

    BP
    Blood pressure regulation :
    HUMORAL

    origin BP

    Plasma & tissue Bradykinin

    BP
    Blood pressure regulation :
    HUMORAL

    BP Bradykinin

    BP = HR x SV x PR

    Angiotensin II Aldosterone Adrenaline ADH

    BP
    2. THE RENIN ANGIOTENSIN SYSTEM /
    KALLICREIN KININ SYSTEM
    Juxtaglomerular apparatus

    Juxtaglomerular cells
    of afferent arteriole

    Macula densa cells


    of distal tubule
    Renin secretion
    BP
    blood volume
    vasodilatation
    Na+ / K+
    sympathetic stimulation

    renin
    renin
    The Renin Angiostensine Aldosterone
    System RAAS/RAS

    Plasma renin angiotensin aldosterone system


    (RAAS)

    Tissue renin angiotensin system


    (RAS)
    Plasma renin angiotensin aldosterone
    system (RAAS)
    BP Renin
    Angiotensinogen Angiotensin I ACE
    AT1
    Angiotensin II
    Adrenal
    AT1 Cortex
    S
    Adrenal Sympathetic
    M
    C
    medulla Stimulation Aldosterone

    VC Adrenaline Na+ /H2O


    reabsorption

    HR, CO BV,SV
    CO
    BP
    Tissue renin angiotensin
    system (RAS)
    Angiotensin I

    Locally produced by several


    ACE
    organs: brain, myocardium,
    kidney, lungs, arteries...
    Angiotensin II
    Angiotensin I is locally
    transformed to Angiotensin II

    Contributes to:
    - vasoconstriction
    - tissue growth
    Angiotensin II

    Angiotensin II

    AT1 AT2
    VC VD
    Aldosterone Antithrombotic
    Sympathetic stimulation Anti growth
    Growth factors Apoptosis
    oxidative stress
    adhesion factors
    PAI-1
    inflammatory factors
    THE KALLICREIN - KININ
    SYSTEM
    The kallicrein-kinin system

    BP
    KININOGEN
    + Kallikrein

    Bradykinin
    ACE + B2 Receptor

    Inactivated Endothelial cell


    Vascular
    smooth
    muscle
    cell

    NO, EDHF, PGI2

    Vasodilation
    BP Growth inhibition
    Bradykinin

    Bradykinin

    B1 B2
    VD
    NO vasodilation
    growth inhibition
    inh of platelet activation
    EDHF
    PGI2
    t PA
    IN SUMMARY

    Angiotensinogen Kininogen

    Renin Kallikrein

    Angiotensin Bradykinin
    I
    + ACE +

    Inactivated
    Angiotensin
    II
    BP BP
    tissue growth tissue growth
    RAAS: a question of balance

    Angiotensine II Bradykinin
    Vasoconstriction Vasodilation
    Adhesion of monocyte cells Antiadhesion of monocytes cells
    Endothelium permeability Restore endothelium
    continuity
    Inflammation
    Antiinflammation
    SMC growth,proliferation
    SMC antigrowth, antiproliferation,
    and migration
    antimigration
    Lipid accumulation
    Reduce lipid accumulation
    Thrombogenesis,
    Fibrinolysis
    Platelet adhesion
    Antiplatelet adhesion

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