Pathophysiology of vascular tone. Arterial hypertension

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Pathophysiology of vascular tone. Arterial
hypertension

• Ph. D., M D. Nataliya Potikha

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Regulation of arterial pressure (?P)
Formula ?P CO PR CO cardiac output PR
peripheral resistance (depended to arterioles
tone)

• CO leads to PR and ?P
  normalizes finally

PR leads to CO and ?P normalizes
finally
AP normal range Systolic 100 - 125
(equilibration 100 - 139) mm Hg Diastolic 70 -
80 (equilibration 60 - 89) mm Hg
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Regulative systems

• 1. Barroreceptors of aorta arch and sinus
  caroticus

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Regulative systems

• 2. Reninangiotensin system

Activation of kidney JGA (juxta glomerular
apparatus)
?P
Excretion of the RENIN (it is enzyme)
Conversation angiotensinogen into angiotensin 1
Conversation angiotensin 1 into angiotensin 2
Angiotensin converting enzyme (?CE)
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Regulative systems

• 3. Reninangiotensin-aldosteron system

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Classification
Arterial hypertension
AP above 139/89 mm Hg
Primary
Secondary

• Arterial hypotension

AP less than 100/60 mm Hg
Acute
Chronic
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Arterial hypertension (?H)

• AP elevation
• (value above 139/89 mm Hg), which is resulted
  from rising of peripheral vessels resistance
• (one of the most common cardiovascular disorders)

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Classification

• Primary AH
• (essential, hypertonic disease)

Secondary AH (that is happened in 5 - 10
cases). Its a symptom of some disease course
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Etiology (primary AH)
Reason is unknown. AH is polyetiological
disease. AH arises on the ground of genetically
peculiarities of metabolism. That is possible
to have genetically defect of the systems, which
control relaxation of the smooth muscle cells of
the arterioles.
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Contributing factors

• Family history

Age-related changes in blood pressure
High salt intake
Stress
Obesity (because hyperinsulinemia)
Excess alcohol consumption (mechanism in unclear)
Hyperinsulinemia causes high activity
sympathetic link of ANS and its effect on cardiac
output, peripheral vascular resistance and renal
sodium retention stimulates sodium and calcium
transport across the cell membrane of vascular
smooth muscle, thereby sensitizing blood vessels
to vasopressor stimuli
Race (for example AH isnt only more prevalent
in African Americans than whites, it is also more
severe). Possible explanation due to
evolutionary adaptation to the severe environment
(western Africa and Western hemisphere) in
condition of salt and water deprivation survival
is possible due to retention of sodium and water
in organism. That leads to conserve sodium.
There is little information about other racial
groups
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Etiologysecondary ?H

• Renal
• (resulted from kidney pathology)

Glomerulonephritis
Kidney damage at collagenosis
Uri stone disease
Kidney amiloidosis
Kidney tumor
Glomerulosclerosis because diabetes mellitus
Nephropathy of the pregnant
Hereditary defect of renal vessels
Renal vessels atherosclerosis, embolism or
thrombosis
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Etiologysecondary ?H
2. Renoprive (arises after kidney remove)
3. Angiogene (is caused by vessels pathology)
Aorta damage
Arteries carotids damage
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Etiologysecondary ?H
4. Endocrinopathy (develops in the result of
endocrine glands pathology)
Acromegaly (Somatotropin over production by the
pituitary gland anterior part)
Hyperaldosteronism (aldosteron over excretion by
suprarenal glands)
Cushing's disease (Adrenocorticotropin over
production by the pituitary gland anterior part)
Menopause (age-depended decrease of female gonads
activity estrogens excretion decrease) Possible
mechanism deficit of NO synthesis by
endotheliocytes
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Etiologysecondary ?H
5. Neurogene (is accompanying to nerves system
pathology)
Encephalitis
Brain tumor
Brain trauma
Brain ischemia
Brain hemorrhage
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Etiologysecondary ?H
6. Cardiac
Heart failure
Heart defect
7. Drug-induced
Drugs, which cause vessels spasm (influent on
kidney), hormonal contraceptives
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Pathogenesis
Increase of circulative blood volume (CBV)

• Emotional excitement
• (SNS activation)

Cardiac output (C?) increase
Peripheral vessels resistance increase
Kidney functions violation
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Pathogenesis
Increase of circulative blood volume (CBV)
NaCl (intake more 5 g/day)
Reasons
Decrease Na excretion by kidney (kidney diseases)
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Pathogenesis
1. CBV increase
Na accumulation in vessels smooth muscle wall and
increase of its osmotic pressure
Na retention in blood
Blood osmotic pressure increase
Vessels wall edema
Vessels smooth muscle sensitivity to
vasoconstrictive influences increase
(noradrenalin, adrenalin, endothelin, angiotensin)
Hypervolemia
Vessels narrowing
Cardiac output increase
Vessels spasm
Peripheral vessels resistance increase
AP elevation
Formula ?P CO PR
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Pathogenesis
2. Cardiac output increase (CO)
Circulative blood volume increase (CBV)
Reasons
Emotional stress
physical (overload) stress
Hyperthyreosis
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Pathogenesis
2. Cardiac output increase
SAS activation
Adrenalin excretion
Increase of cardiac contractility force
Increase of heart beats
Increase of cardiac output
AP elevation
Formula ?P CO PR
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Pathogenesis
3. SAS activation
SAS activation
Suprarenal glands activation
Interaction adrenalin and alpha-adrenoreceptors
Venues smooth muscles spasm
Arterioles smooth muscles spasm
Increase of circulative blood in big blood circle
?drenalin
Noradrenalin
adrenoreceptors of heart
alpha-adrenoreceptors of vessels
Arterioles narrowing
Increase of CBV
Arterioles narrowing
PR increase
CO increase
CO increase
AP increase
Formula ?P CO PR
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Pathogenesis
4. Kidney functions violation
Long time spasm of kidneys arteries

• Angiotensin 2 effects
• Smooth muscles contraction in the vessels
• Stimulation of the vasoactive center in brain
• Noradrenalin excretion increase
• Adrenalin excretion increase from suprarenal
  glands
• Aldosteron excretion increase from suprarenal
  glands (Na retention due to kidney)

AP decrease in renal capillaries
Activation of JGA
Renin excretion
Angiotensin 2 synthesis
AP increase
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Depressive function of kidney synthesis of the
substances for AP reduce
dilates renal arteries, reduces renin synthesis
and reduces Na reabsorbing in kidney
PG ? 2
! ! ! Exhaustion of kidney depressive function
leads to arterial hypertension stabilization
Phospholipid Renin Inhibitor
Angiotensinase
Phosphatydilcholin alkali ethers
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Arterial hypertension after-effects
1st period functional violations (heart
hypertrophy)

• 2d period
• Pathological changes in arteries and arterioles
  (dystrophy)
• Arterioles sclerosis
• Arterioles wall infiltration by plasma (leads to
  dystrophy)
• Arterioles necrosis (hypertonic crisis arises in
  clinic)
• Veins wall thickening

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Arterial hypertension after-effects
3d period Secondary changes in organs and systems
CNS brain hypoxia neurons destruction
apoplexy (because vessels destruction and rupture
leads to brain hemorrhages and brain destruction)
Kidney (nephrosclerosis and chronic kidney
insufficiency)

• Organs of vision
• retinopathy (retinas vessels injury)
• hemorrhages and separation (exfoliation) of
  retina, that leads to blindness

Heart Decompensate heart failure
Endocrine system Glands atrophy and sclerosis
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Retinopathy