Regulation of Visceral Activity4
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Transcript of 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