Pathophysiology of vascular tone. Arterial hypertension

Ph. D., M D. Nataliya Potikha

Regulation of arterial pressure (АP)

Formula: АP = CO · PRCO – cardiac output

PR – peripheral resistance (depended to arterioles tone)

CO leads to PR and АP normalizes finally

PR leads to CO and АP normalizes finally

AP normal range:

Systolic – 100 - 125 (equilibration 100 - 139) mm Hg

Diastolic – 70 - 80 (equilibration 60 - 89) mm Hg

Regulative systems

1. Barroreceptors of aorta arch and sinus caroticus

Barroreceptors of the vessels

Medulla oblongata (vessel’s active center)

Afferent impulses

Heart (CO increase at decreased АP)

Arterioles (spasm) Еfferent і impulses

Regulative systems

2. Renin–angiotensin system

АPActivation of kidney

JGA (juxta glomerular apparatus)

Excretion of the RENIN

(it is enzyme)

Conversation

angiotensin 1 into angiotensin 2

Conversation angiotensinogen into angiotensin 1

Angiotensin converting enzyme (АCE)

Regulative systems

3. Renin–angiotensin-aldosteron system

Renin Actination of suprarenal glangs

(cortical layer)

Na reabsorbtion

in kidney increase

Angiotensin 2

Aldosteron excretion

Na concentration in blood increase,

blood osmotic pressure increase

Move of extravascular fluid inside the

vessels

Increase of circulative blood volume

(CBV)

CО increase

Classification

Arterial hypotension

Arterial hypertension

AcuteChronic

Secondary

AP above 139/89 mm Hg

Primary

AP less than 100/60 mm Hg

AP elevation (value above 139/89 mm Hg), which is resulted from rising

of peripheral vessels resistance

(one of the most common cardiovascular disorders)

Arterial hypertension (АH)Arterial hypertension (АH)

Classification

Primary AH (essential, hypertonic disease)

Secondary AH (that is happened in 5 - 10 % cases).

It’s a symptom of some disease course

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.

Etiology (primary AH) Etiology (primary AH)

Contributing factorsFamily history

Age-related changes in blood pressureHigh salt intake

Stress

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

Obesity (because hyperinsulinemia)Excess alcohol consumption

(mechanism in unclear)

Race

(for example: AH isn’t 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

1. Renal (resulted from kidney pathology)

Etiologysecondary АHEtiologysecondary АH

GlomerulonephritisGlomerulonephritis

Kidney damage at collagenosis

Kidney damage at collagenosis

Kidney amiloidosisKidney amiloidosis

Glomerulosclerosis because diabetes mellitus

Glomerulosclerosis because diabetes mellitus

Nephropathy of the pregnant

Nephropathy of the pregnant

Hereditary defect of renal vessels

Hereditary defect of renal vessels

Renal vessels atherosclerosis, embolism or thrombosis

Renal vessels atherosclerosis, embolism or thrombosis

Kidney tumorKidney tumor

Uri stone diseaseUri stone disease

3. Angiogene(is caused by vessels pathology)

2. Renoprive (arises after kidney remove)

Etiologysecondary АHEtiologysecondary АH

Aorta damageAorta damage Arteries carotids damage

Arteries carotids damage

4. Endocrinopathy (develops in the result of endocrine glands pathology)

Etiologysecondary АHEtiologysecondary АH

Cushing's disease (Adrenocorticotropin over production by

the pituitary gland anterior part)

Cushing's disease (Adrenocorticotropin over production by

the pituitary gland anterior part)

Acromegaly (Somatotropin over production by

the pituitary gland anterior part)

Acromegaly (Somatotropin over production by

the pituitary gland anterior part)

Hyperaldosteronism (aldosteron over excretion by suprarenal

glands)

Hyperaldosteronism (aldosteron over excretion by suprarenal

glands)

Menopause(age-depended decrease of female

gonads activity – estrogens excretion decrease)

Possible mechanism – deficit of NO synthesis by endotheliocytes

Menopause(age-depended decrease of female

gonads activity – estrogens excretion decrease)

Possible mechanism – deficit of NO synthesis by endotheliocytes

5. Neurogene (is accompanying to nerves system pathology)

Etiologysecondary АHEtiologysecondary АH

Brain hemorrhageBrain hemorrhage

EncephalitisEncephalitis

Brain tumorBrain tumor

Brain traumaBrain trauma

Brain ischemiaBrain ischemia

7. Drug-induced

6. Cardiac

Etiologysecondary АHEtiologysecondary АH

Heart failureHeart failureHeart defectHeart defect

Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives

Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives

Emotional excitement (SNS activation)

Emotional excitement (SNS activation)

Increase of circulative blood volume (CBV)Increase of circulative blood volume (CBV)

Cardiac output (CО) increaseCardiac output (CО) increase

Kidney functions violationKidney functions violation

Peripheral vessels resistance increasePeripheral vessels resistance increase

Pathogenesis

Increase of circulative blood volume (CBV)Increase of circulative blood volume (CBV)

Pathogenesis

Reasons

NaCl (intake more 5 g/day) NaCl (intake more 5 g/day)

Decrease Na excretion by kidney

(kidney diseases)Decrease Na excretion by kidney

(kidney diseases)

1. CBV increase1. CBV increase

Na retention in bloodNa retention in blood

Blood osmotic pressure increase

Blood osmotic pressure increase

HypervolemiaHypervolemia

Cardiac output increaseCardiac output increase

AP elevationAP elevation

Na accumulation in vessels smooth muscle wall and increase of its

osmotic pressure

Na accumulation in vessels smooth muscle wall and increase of its

osmotic pressure

Vessels wall edemaVessels wall edema

Vessels narrowingVessels narrowing

Peripheral vessels resistance increasePeripheral vessels

resistance increase

Vessels smooth muscle sensitivity to

vasoconstrictive influences increase

(noradrenalin, adrenalin, endothelin, angiotensin)

Vessels smooth muscle sensitivity to

vasoconstrictive influences increase

(noradrenalin, adrenalin, endothelin, angiotensin)

Formula: АP = CO · PRFormula: АP = CO · PR

Pathogenesis

Vessels spasm

Vessels spasm

2. Cardiac output increase (CO)2. Cardiac output increase (CO)

Reasons

Circulative blood volume increase (CBV)

Circulative blood volume increase (CBV)

physical (overload) stress

physical (overload) stress

Emotional stress Emotional stress

HyperthyreosisHyperthyreosis

Pathogenesis

2. Cardiac output increase2. Cardiac output increase

SAS activationSAS activation

Adrenalin excretionAdrenalin excretion

Increase of cardiac contractility force

Increase of cardiac contractility force

Increase of cardiac output

Increase of cardiac output

Increase of heart beats Increase of heart beats

AP elevationAP elevation

Pathogenesis

Formula: АP = CO · PRFormula: АP = CO · PR

3. SAS activation3. SAS activation

Interaction adrenalin and alpha-adrenoreceptors

Interaction adrenalin and alpha-adrenoreceptors

Arterioles smooth muscles spasm

Arterioles smooth muscles spasm

Suprarenal glands activation

Suprarenal glands activation

Venues smooth muscles spasm

Venues smooth muscles spasm

Increase of circulative blood in big blood

circle

Increase of circulative blood in big blood

circle adrenoreceptors of

heartadrenoreceptors of

heart

АdrenalinАdrenalinNoradrenalinNoradrenalin

Increase of CBVIncrease of CBV

CO increaseCO increase

Arterioles narrowing

Arterioles narrowing

alpha-adrenoreceptors of vessels

alpha-adrenoreceptors of vessels

CO increaseCO increase

AP increaseAP increase

SAS activationSAS activation

Arterioles narrowing Arterioles narrowing

PR increasePR increase

Pathogenesis

Formula: АP = CO · PRFormula: АP = CO · PR

4. Kidney functions violation4. Kidney functions violation

Long time spasm of kidney’s arteries

Long time spasm of kidney’s arteries

AP increaseAP increase

AP decrease in renal capillaries

AP decrease in renal capillaries

Activation of JGAActivation of JGA

Renin excretionRenin excretion

Angiotensin 2 synthesis

Angiotensin 2 synthesis

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)

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)

Pathogenesis

Depressive function of kidney – synthesis of the substances for AP reduce

Depressive function of kidney – synthesis of the substances for AP reduce

PG Е 2PG Е 2

Phospholipid Renin Inhibitor

Phospholipid Renin Inhibitor

AngiotensinaseAngiotensinase

Phosphatydilcholin alkali ethers

Phosphatydilcholin alkali ethers

! ! !

Exhaustion of kidney depressive function

leads to arterial hypertension stabilization

dilates renal arteries, reduces renin synthesis and reduces Na

reabsorbing in kidney

dilates renal arteries, reduces renin synthesis and reduces Na

reabsorbing in kidney

1st period

functional violations

(heart hypertrophy)

2d periodPathological changes in arteries and arterioles (dystrophy):- Arterioles sclerosis

- Arteriole’s wall infiltration by plasma (leads to dystrophy)

- Arterioles necrosis (hypertonic crisis arises in clinic)

- Vein’s wall thickening

Arterial hypertension after-effects

3d period

Secondary changes in organs and systems

Kidney

(nephrosclerosis and chronic kidney insufficiency)

Kidney

(nephrosclerosis and chronic kidney insufficiency)

CNS

– brain hypoxia

– neurons destruction

– apoplexy (because vessels destruction and rupture leads to brain hemorrhages and brain destruction)

CNS

– brain hypoxia

– neurons destruction

– apoplexy (because vessels destruction and rupture leads to brain hemorrhages and brain destruction)

Heart

Decompensate heart failureHeart

Decompensate heart failure

Organs of vision- retinopathy (retina’s vessels injury)- hemorrhages and separation (exfoliation) of

retina, that leads to blindness

Organs of vision- retinopathy (retina’s vessels injury)- hemorrhages and separation (exfoliation) of

retina, that leads to blindness

Endocrine system

Glands atrophy and sclerosisEndocrine system

Glands atrophy and sclerosis

Arterial hypertension after-effects

Retinopathy