regulation of visceral activity4

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    REGULATION OF VISCERALACTIVITYWAYNE MANANA

    BDS(UZ),BA,MDS(OMFS)

    FACILITATOR ; DR W. MURITHI

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    COMPONENTS OF A CONTROLLED

    SYSTEM

    sensor

    Afferent pathway

    Controller/ intergrator Efferent pathway

    Effector

    Controlled variable

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    Mechanisms of visceral activity control

    Can be

    Negative feedback(most common)

    Positive feedback e.g release of cck, secretin

    Feedforward e.g exercise, salivation, gastric secretion

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    Can also be

    Involuntary/ automatic

    voluntary

    Can be

    Endocrine

    Paracrine

    Neuronal/ nervous

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    Major visceral activity

    Cardiovascular system

    Respiratory system

    Gastrointestinal system Renal system

    Genitourinary system

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    LEVELS OR HIERACHY OF

    REGULATION

    Spinal cord

    Bladder reflexes

    Medulla(vital centres)

    CVS and RS

    Vomiting, coughing, gagging, sneezing, swallowing

    Hypothalamus

    Satiety, hunger, thirst, Midbrain-pupillary and accommodation reflexes

    Basal nuclei and cortex-modulation of brain stem

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    Spinal cord(defecation/voiding)

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    MEDULLARY LEVEL

    REGULATION OF CVS

    Can be

    Neural(rapid pressure changes e.g postural changes)

    Endocrine( delayed response)

    paracrine

    Regulation occurs at

    Local tissue level(autoregulation)

    Systemic/ general

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    CONTROLLED VARIABLES

    Blood pressure

    Oxygen and nutrients to the tissues

    Carbon dioxide, H+, metabolites from tissues

    Temperature(thermoregulation)

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    Receptors cvs

    Baroreceptors

    Stretch receptors in the tunica adventia

    High pressure baroreceptors

    Carotid sinus Aortic arch receptors

    Low pressure baroreceptors(cardiopulmonaryreceptors)

    Rt and lt atrium(Type A and Type B) receptors Pulmonary vessels receptors

    Ventricular walls

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    Baroreceptors cont

    More sensitive to pulsatile pressure than to constant

    pressure

    Chronic hypo/hypertension resetsthe

    baroreceptors

    Carotid sinus- linear relationship in response

    between 70 and 150mmHg

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    chemoreceptors

    Peripheral chemoreceptors mainly exert their effect

    on resp system but their stimulation also causes

    vasoconstriction

    Hypoxia produces hyperpnea and increases

    catecholamine release

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    Afferent pathway

    Carotid sinus

    Glossopharyngeal(carotid sinus nerve)

    Aortic arch

    Vagus(aortic depressor nerve)

    Neurotransmitter

    glutamate

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    Basic pathways; medullary bp control

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    Medullary control of heart rate by

    vagus

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    Other afferents to th RVLM

    excitatory

    Limbic cortex that relay in the hypothalamus

    Mesencephalic periaquaductal gray

    Brainstem reticular formation

    Pain pathways

    Somatic afferent(somatosympathetic reflex..exercise)

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    Afferent cont..

    Inhibitory

    Cortex via hypothalamus

    Caudal medullary raphe

    Lung inflation afferents

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    Efferent and effector

    ANS to smooth muscles(mainly arterioles) via

    endothelial cells

    Ach binds to end cells and they is increased

    intracellular calcium which activate NOS3 which

    activates guanyly cyclase then relaxation smooth

    muscle

    Expt capillaries and venules Noradrenegic expt muscles

    Cardiac receives both PS and S

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    autoregulation

    Myogenic theory of autoregulation

    Metabolic theory of autoregulation

    Stagnation built-up of metabolites

    Metabolites have vasodilator effect e.g low O2, Low

    pH, inreases CO2, hyperosmolarity, rise in temp,

    hyperkalaemia a feature, lactate, histamine, adenosine,

    NO(EDRF),bradykinin, CO

    vasoconstriction 5-HT from plts in injured,histamine via

    H1, sub P, VIP, ET

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    REGULATION OF RS

    Can be voluntary or involuntary

    Can be neuronally or chemically controlled

    The controlled variable is pO2, pCO2 and pH

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    chemoreceptors

    Chemoreceptors

    Carotid bodies (more important)

    Aortic bodies

    Medullary chemoreceptors(R/CVM)

    Close to NTS,hypothalamus, locus ceruleus

    Glomus cells(type 1) with K+-sensitive O2

    channels and L-type Ca2+ channels Stimulated by low O2, CN-,nicotine, lobeline,

    hyperkalaemia,

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    Non-chemical receptors

    Myelinated

    Slow adapting type(herring-breuer relexes)

    Rapidly adapting type(irritant receptors)

    Non-myelinated(J receptors)

    Pulmonary C fibers

    Bronchial C fibers

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    afferent

    Afferent Vagus (aortic body and the non-chemical receptors)

    Glossopharyngeal (carotid body)

    Have D2 receptors

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    contollers

    4 contollers

    Pre-BOTC

    Dorsal and Ventral

    groups of resp

    Pneumotaxic centre

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    DRG and VRGbothfound in the medulla andproject to the pre-BOTC

    Pneumataxic center

    modifies the Pre-BOTC.PC located in the medialparabrachial and kollikernuclei of th dorsolat pons

    PC fxn not known butprobably switchingbtwn insp and exp

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    OTHER AFFERENTS

    Reticular formation

    Propioceptors

    Limbic system, hypothalamus

    Baroreceptors

    Cerebral cortex

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    efferents

    Voluntary

    Corticospinal to accesory muscles of resp and

    intercostal muscles

    Automatic

    Cervical via phrenic nerve goes to the diaphragm

    Thoracic via intercostal nerves goes th intercostal

    muscles

    Sympathetic(B2) causes brochodilation & vasoC

    Parasymp(vagus) opposes symp

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    COUGHING AND SNEEZING

    Triggered my irritation of resp mucosa

    Coughing begins by deep insp followed by forced

    exp.

    Intrapulmonary pressure increases to 100mmHg or

    more, glottis open, outflow at 965km/hr(600mi/hr)

    Sneezing similar expt glottis continuosly open and

    initiated by pain fibers of trigeminal nerve(nasalepithelium)

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    REGULATION OF GIT

    Regulation can be

    neural,(intrinsic and extrinsic)

    endocrine and paracrine

    Controlled variable is secretion and motility with an

    ultimate goal of efficient digestion, absorption and

    assimilation

    Git like the little brain

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    Regulation of salivation(prototype for

    glands)

    Feed forward andfeedback

    Symp alpha-1causes thick viscous,Beta causesamylase secretion

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    vomiting

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    HYPOTHALAMUS LEVEL

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    VISCERAL FUNCTION OF

    HYPOTHALAMUS

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    FUNCTIONS CONT..

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    Role of hypothalamus in;

    Posterior pituitary(oxytocin/VP)

    Appetitive mechanisms

    Hunger and satiety

    thirst

    Relation to

    Autonomic function

    Cyclic phenomenon

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    HUNGER AND SATIETY

    Appetite depends on interaction btwn

    Satiety centre(ventromedial nucleus)

    Feeding centre(bed nucleus of forebrain bundle at its

    junction with the pallidohypothalamic fibres)

    Leptin and more 20 proteins/pptides have been

    implicated in the regulation of appetite

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    HUNGER AND SATIETY

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    AFFERENT MECHANISMS HYPOTHESIS

    Lipostatic hypothesis

    Humoral signal(leptin) from adipose produced

    proportional to fat, acts on hypoTh to inhib apt

    Gut peptide hypothesis

    Food in GIT stimulates hormones to inhib hypoTh

    Glucostatic hypothesis

    Thermostatic hypothesis Fall in temp below set pt stimulate apt and vice versa

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    LEPTIN (lipostatic hypothesis)

    167aas, o/b gene(leptin)and d/b gene(receptor)

    Acts on the hypoTh todecrease food intake by

    Decrease th activity ofneuropepptide Y neurons

    Increase th activity of POMCfrom neurons

    Leptin acts on arcuate

    nuclei(can be destroyed bygold thioglucose)

    Competes for CB1 receptorwth cannabinoids

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    GHRELIN

    28 aas pptide wth n-

    octanyl on serine 3

    residues

    Antagonizes the action ofleptin

    Produced by stomach to

    act on th arcuate nuclei to

    stimulate appetite

    Stimulates GH release

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    Other peptides

    Peptide YY3-26(PYY)

    From small intestines and colon to inhibit appetite

    GIT hormones

    CCK, secretin, somatostatin, gastrin, GRP

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    THIRST

    Triggered by hypovolaemia

    hyperosm

    Psychological

    Osmoreceptors located in thant hypoTh in thcircumventricular organs

    subfornical organ and OVLThave receptors forAngiotensin II

    Baroreceptor reflexmechanisms also involved intriggering thirst in

    hypovoelemic patients

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    Thirst-osmolarity relationship

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    Other factors affecting water intake

    Prandial water drinking

    Psychological/ habit

    Increased plasma osmolarity

    GIT hormones acting on the hypothalamus

    Ant cerebral artery injuries,lesions in the ant hypoTh,

    altered state of unconsciousness, high protein diet,

    pharyngeal mucosa drying Pharyngeal gastrointestinal metering probably

    involved in satisfaction of thirst

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    CONTROL OF POST PITUITARY FXN

    OXYTOCIN AND VASOPRESSIN Nonapptides neural hormones

    with terminal disulphide ring

    Synthesized by magnocellularneurons(Herring bodies

    granules) in theparaventricular and supra-optic nuclei

    Other species have lysine-VP

    Also found in gonads,

    thymus,adrenal cortex,suprachiasmatic N, brainstem& spinal cord(T.boutons)

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    CHEMISTRY OF VP AND OXYTOCIN

    An AP in the magnocellular neurons triggers a Ca2+

    mediated exocytosis of both VP and oxytocin

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    Physiologic action of VP

    Release is phasic bursting non-synchronous and

    mantains a prolonged output increase in VP

    Causes water retention in excess of solute by acting

    on collecting duct

    VIAReceptors

    G protein coupled to increase IC Ca2+ and mediates

    vasoC.(at high levels because at low level causes adecrease in CO by acting on th area postrema)

    Also found in the liver(glycogenolysis), brain&cord(NT)

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    Receptors cont

    V1B(also calledV3)is a G protein coupled to

    increase IC Ca2+ found in the ant pituitary to

    release ACTH.

    V2 receptor

    is a Gs protein coupled that triggers to increase cAMP

    found on the principal cells of the collecting duct

    Facilitates insertion of aquaporin-2 into the apicalmembrane

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    Relationship btwn osm/BP and VP

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    VP

    T1/2 of18mins andinactivated in the liver

    Regulated by OVLT

    receptors but the

    threshold for thirst is

    slightly higher

    Significant changes

    occur even if osmchanges by 1%

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    oxytocin

    Acts via G protein coupled receptors on themyometrium, breast myoepithelial cells and ovary totrigger increase in I.C Ca2+ .

    Milk ejection reflex(neuroendocrine reflex)Many hormones cause breast growth and secretion but

    ejection is entirely due to oxytocin

    Tactile/stretch receptors on the nipple trigger a high

    frequency, synchronous discharge of Oxytocin Emotions and genital stimulation stimulate release but

    alcohol inhib

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    Other actions of oxytocin

    Stimulate uterine contraction. Inhibited by

    progesterone(competitive inhib on oxytocin

    receptors) and activated by estrogen

    Coitus stretch stimulate uterine contraction tofacilitate mvnt of sperm.

    circulating levels elevated at ejaculation ???

    contraction of vas deferens smooth muscle??

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    QUOTE OF THE DAY

    WHAT IS NOT WORTH DYING FOR IS NOT

    WORTHY LIVING FOR

    HYPOTHALAMUS REGULATES BUT GOD

    CONTROLS