This document discusses blood vessel pathology and blood pressure regulation. It covers the nervous and hormonal factors involved in both rapid and long-term blood pressure control. The renin-angiotensin-aldosterone system and its role in blood pressure regulation is explained. Causes, risk factors, pathogenesis and complications of both primary and secondary hypertension are described. Treatment involves controlling blood pressure to prevent target organ damage.

1. Blood vessels pathologyBlood vessels pathology

2. Blood pressure regulationBlood pressure regulation
BP
Cardiac
Output
Peripheral
Resistance
Renal
control system
Neural Factors
Humoral Factors

3. Blood pressure regulationBlood pressure regulation
TheThe increase of BPincrease of BP::
 sympathetic nervous systemsympathetic nervous system
 humoral factors (rennin-angiotensin-aldosteronehumoral factors (rennin-angiotensin-aldosterone
system, vasopressine, glucocorticoids)system, vasopressine, glucocorticoids)
 kidney and fluid balance mechanismskidney and fluid balance mechanisms

4. Blood pressure regulationBlood pressure regulation
TheThe decrease of BPdecrease of BP ::
 baroreceptor reflexes from aorta arch andbaroreceptor reflexes from aorta arch and
carotid sinuses.carotid sinuses.
 prostoglandins A, E, Iprostoglandins A, E, I
 kallikrein –kinin systemkallikrein –kinin system
 atriumatrium natriuretic factornatriuretic factor

5. Rapid pressure controlRapid pressure control
Nervous reflexes mechanismsNervous reflexes mechanisms
 BaroreceptorsBaroreceptors control BP in posture change, exercise,control BP in posture change, exercise,
and moderate temperature changesand moderate temperature changes
 Sympathetic activitySympathetic activity - increased heart rate, and- increased heart rate, and
cardiac contractility, vasoconstriction, increased BPcardiac contractility, vasoconstriction, increased BP
 Parasympathetic activityParasympathetic activity produces the oppositeproduces the opposite
motor responses.motor responses.
 Cardiopulmonary receptorsCardiopulmonary receptors - vasoconstriction,- vasoconstriction,
tachycardia.tachycardia.
 ChemoreceptorsChemoreceptors (pH, blood gases, changes in plasma(pH, blood gases, changes in plasma
composition) - vasoconstriction and bradycardia.composition) - vasoconstriction and bradycardia.

6. Rapid pressure controlRapid pressure control
Hormonal mechanismsHormonal mechanisms
 Norepinephrine/epinephrineNorepinephrine/epinephrine ––
vasoconstriction, increased heart ratevasoconstriction, increased heart rate
 VasopressinVasopressin - vasoconstriction.- vasoconstriction.
 Renin-angiotensin-aldosteroneRenin-angiotensin-aldosterone systemsystem

7. Renin-angiotensin-aldosteroneRenin-angiotensin-aldosterone
systemsystem
angiotensin-converting enzyme is present
in the endothelium of the lung vessels.
Angiotensin II:
• vasoconstrictor response
increases TPVR and BP (short-
term regulation)
•stimulation of aldosterone
secretion (long term regulation)
Aldosterone causes salt and water
retention (increase of blood
volume and BP).

8. Long-term regulation of BPLong-term regulation of BP
Renal regulationRenal regulation
 Water resorption - aldosterone andWater resorption - aldosterone and
vasopressinvasopressin
 Sodium retention - aldosterone.Sodium retention - aldosterone.
 An increase in renal output - decrease inAn increase in renal output - decrease in
venous return and arterial pressure.venous return and arterial pressure.
  in extracellular volume withoutin extracellular volume without
compensation from the kidneys - high BPcompensation from the kidneys - high BP..

9. Long-term regulation of BPLong-term regulation of BP
Extracellular
fluid volume
BP
 cardiac output
excessive bloodflow
in tissues
vasoconstriction

10. Classification of arterialClassification of arterial
hypertensionhypertension
CategoryCategory Systolic BPSystolic BP
(mm hg)(mm hg)
Diastolic BPDiastolic BP
(mm hg)(mm hg)
Normal BPNormal BP Below 130Below 130 Below 85Below 85
High-normal BPHigh-normal BP
(pre-hypertension)(pre-hypertension)
130-139130-139 85-8985-89
Stage 1 (mild) hypertensionStage 1 (mild) hypertension 140-159140-159 90-9990-99
Stage 2 (moderate) hypertensionStage 2 (moderate) hypertension 160-179160-179 100-109100-109
Stage 3 (severe) hypertensionStage 3 (severe) hypertension 180 or higher180 or higher 110 or higher110 or higher

11. Arterial hypertensionArterial hypertension
Primary hypertensionPrimary hypertension (90%)(90%) --
without evidence of other diseaseswithout evidence of other diseases
multifactorial syndromemultifactorial syndrome
increased TPVRincreased TPVR
Secondary hypertensionSecondary hypertension (10%)(10%)
depends on other diseases (kidneys, endocrine etc.)depends on other diseases (kidneys, endocrine etc.)

12. Factors contributing toFactors contributing to
primary hypertensionprimary hypertension
 StressStress
 Increased sympathetic activityIncreased sympathetic activity
 Stress-induced vasoconstrictionStress-induced vasoconstriction
 Genetic factorsGenetic factors
 familiar cases of hypertension,familiar cases of hypertension,
 identification of gene responsible for hypertensionidentification of gene responsible for hypertension
 Racial and environmental factorsRacial and environmental factors
 Black race -higher incidence of essential hypertensionBlack race -higher incidence of essential hypertension
 salt intake (due tosalt intake (due to  blood volume, sensitivity of CVS toblood volume, sensitivity of CVS to
adrenergic influences)adrenergic influences)

13. Risk factors modifying the course ofRisk factors modifying the course of
essential hypertensionessential hypertension
 age (in younger persons more severe)age (in younger persons more severe)
 sex (premenopausal females have bettersex (premenopausal females have better
prognosis)prognosis)
 atherosclerosis (impairs vessels elasticity)atherosclerosis (impairs vessels elasticity)
 smoking,, excess of alcohol intakeof alcohol intake
 diabetes mellitus and insulin-resistancediabetes mellitus and insulin-resistance

14. Insulin resistance and hypertensionInsulin resistance and hypertension
part ofpart of syndrome X, or the metabolic syndromesyndrome X, or the metabolic syndrome whichwhich
includesincludes::
 central obesity,central obesity,
 dyslipidemia (especially elevated triglycerides),dyslipidemia (especially elevated triglycerides),
 insulin resistance and/or hyperinsulinemia
 high blood pressure.high blood pressure.
Hyperinsulinemia can increase BPHyperinsulinemia can increase BP::
 produces renal sodium retention (at least acutely) andproduces renal sodium retention (at least acutely) and
increases sympathetic activity.increases sympathetic activity.
 mitogenic action of insulin promotes is vascularmitogenic action of insulin promotes is vascular
smooth-muscle hypertrophy increasing TPVRsmooth-muscle hypertrophy increasing TPVR

15. Secondary hypertensionSecondary hypertension
Renal hypertensionRenal hypertension
 from chronicfrom chronic
kidneys diseaseskidneys diseases Renin by JGA
Angiotensin II
Vasoconstriction
↑ P. Resistance
Sodium Retention
↑Blood Volume
Aldosterone
Hypertension
Decreased glomerular filtration rate

16. Etiology of secondaryEtiology of secondary
hypertensionhypertension
 ↑↑secretion ofsecretion of aldosteronealdosterone
 Cushing’s syndrome/disease -Cushing’s syndrome/disease - ↑↑ glucocorticoidglucocorticoid
secretion.secretion.
 Phaeochromocytoma - tumour releasing bothPhaeochromocytoma - tumour releasing both
noradrenaline and adrenalinenoradrenaline and adrenaline..
 PregnancyPregnancy (the last 3 months)(the last 3 months)
 DrugsDrugs (steroids, oral contraceptives, sympatomimetics,(steroids, oral contraceptives, sympatomimetics,
aldosterone, and vasopressin).aldosterone, and vasopressin).
 Cardiovascular disorder (Cardiovascular disorder (coarctation of the aortacoarctation of the aorta) - low) - low
pressure distal to the coarctation.pressure distal to the coarctation.
 AtherosclerosisAtherosclerosis

17. Hypertension pathogenesisHypertension pathogenesis
 Stress, hypodynamiaStress, hypodynamia  sympathetic overactivitysympathetic overactivity
 increased cardiac outputincreased cardiac output..
 Episodes of high BPEpisodes of high BP  increase of TPVRincrease of TPVR
 increase of TPVRincrease of TPVR  glomerular filtrationglomerular filtration 
renin-angiotensin-aldosterone cascaderenin-angiotensin-aldosterone cascade
increased NaCl/water retentionincreased NaCl/water retention..
 increased vascular tone results in a rise in TPVRincreased vascular tone results in a rise in TPVR

18. Hypertension pathogenesisHypertension pathogenesis
Vicious circle of hypertensionVicious circle of hypertension
High BP
Hyperthrophy
of arterioles
smooth muscles
 TPVR

19. Hypertension pathogenesisHypertension pathogenesis
 Deficiency of vasodilator substancesDeficiency of vasodilator substances
 bradykinin from kinin-kallikrein systembradykinin from kinin-kallikrein system
 neutral lipid and prostaglandin from renalneutral lipid and prostaglandin from renal
parenchymaparenchyma
 renoprival hypertension in anephric personsrenoprival hypertension in anephric persons
 Endothelial dysfunctionEndothelial dysfunction
 Imbalance between endothelin and NO,Imbalance between endothelin and NO,
prostacyclinprostacyclin

20. Hypertension signs andHypertension signs and
symptomssymptoms
Primary hypertension is asymptomatic untilPrimary hypertension is asymptomatic until
complications developcomplications develop in target organs.in target organs.
HeartHeart
 left ventricule hypertrophyleft ventricule hypertrophy
 angina pectorisangina pectoris
 myocardial infarctionmyocardial infarction
 heart failure

21. Hypertension signs andHypertension signs and
symptomssymptoms
 HypertensiveHypertensive retinopathyretinopathy - retinal- retinal
hemorrhages, exudates, vascular accidents.hemorrhages, exudates, vascular accidents.
 HypertensiveHypertensive encephalopathyencephalopathy - dizziness,- dizziness,
headache, fatigue, nervousness.headache, fatigue, nervousness.
 Brain strokeBrain stroke – ischemic and hemmorrhagic– ischemic and hemmorrhagic
 HypertensiveHypertensive nephropathynephropathy - chronic renal- chronic renal
failure due to chronically high bloodfailure due to chronically high blood
pressure.pressure.

22. Hypertension treatmentHypertension treatment
Primary hypertension cannot be cured, but it can bePrimary hypertension cannot be cured, but it can be
controlled to prevent complications.controlled to prevent complications.
 Losing weight.Losing weight.
 Changes in diet.Changes in diet.
 Stop smoking.Stop smoking.
 Reducing the intake of alcohol and sodium.Reducing the intake of alcohol and sodium.
 Moderate regular aerobic exercise.Moderate regular aerobic exercise.
 If modification of lifestyle in 6 months was notIf modification of lifestyle in 6 months was not
successful, antihypertensive drugs are prescribed.successful, antihypertensive drugs are prescribed.

23. Arterial hypotensionArterial hypotension
Neurogenic causesNeurogenic causes - autonomic dysfunction or failure:- autonomic dysfunction or failure:
 central nervous system abnormalities (Parkinson’s disease)central nervous system abnormalities (Parkinson’s disease)
 secondary to systemic diseases (diabetes, vasovagalsecondary to systemic diseases (diabetes, vasovagal
hyperactivity).hyperactivity).
Nonneurogenic causesNonneurogenic causes of hypotensionof hypotension
 vasodilation (alcohol, drugs, fever)vasodilation (alcohol, drugs, fever)
 cardiac disease (cardiomyopathy, valvular disease);cardiac disease (cardiomyopathy, valvular disease);
 reduced blood volume (hemorrhage, dehydration, or otherreduced blood volume (hemorrhage, dehydration, or other
causes of fluid loss.causes of fluid loss.

24. Orthostatic or postural hypotensionOrthostatic or postural hypotension
 is an abnormal drop in BP on assumption of theis an abnormal drop in BP on assumption of the
standing position.standing position.
 normally, it is compensated by increase in heart ratenormally, it is compensated by increase in heart rate
 Weakness, dizziness, syncope (i.e., fainting),Weakness, dizziness, syncope (i.e., fainting),
 common complaints of elderly persons.common complaints of elderly persons.
ССausesauses
 ANS dysfunctionANS dysfunction
 reduced blood volume– dehydration (diuretics,reduced blood volume– dehydration (diuretics,
excessive diaphoresis, loss of gastrointesinal fluidsexcessive diaphoresis, loss of gastrointesinal fluids
through vomiting and diarrhea).through vomiting and diarrhea).

25. Hypotension treatmentHypotension treatment
 Avoidance of factors that can precipitate hypotensionAvoidance of factors that can precipitate hypotension
 sudden changes in posture,sudden changes in posture,
 hot environments,hot environments,
 alcohol,alcohol,
 certain drugs,certain drugs,
 large meals.large meals.
 Volume expansion (using salt supplements and/orVolume expansion (using salt supplements and/or
medications with salt-retaining properties),medications with salt-retaining properties),
 Mechanical measures (to prevent the blood fromMechanical measures (to prevent the blood from
pooling in the veins of the legs upon standing).pooling in the veins of the legs upon standing).

26. AtherosclerosisAtherosclerosis
Atherosclerosis is a process of progressive lipidis a process of progressive lipid
accumulation with the formation of multiple plaquesaccumulation with the formation of multiple plaques
within the arteries.within the arteries.
 Atherosclerotic plaque containsAtherosclerotic plaque contains
 lipidslipids
 inflammatory cellsinflammatory cells
 smooth muscle cells,smooth muscle cells,
 connective tissueconnective tissue
 thrombi,thrombi,
 CaCa2+2+
deposits.deposits.

27. AtherosclerosisAtherosclerosis
 ArteriosclerosisArteriosclerosis - any hardening (and loss of- any hardening (and loss of
elasticity) of medium or large arterieselasticity) of medium or large arteries
 ArteriolosclerosisArteriolosclerosis - affectiong of the arterioles- affectiong of the arterioles
(small arteries)(small arteries)
 AtherosclerosisAtherosclerosis is a hardening of an arteryis a hardening of an artery
specifically due to anspecifically due to an atheromatous plaqueatheromatous plaque (in(in
Greek, "athero" means "porridge").Greek, "athero" means "porridge").
 Atherosclerosis is a form of arteriosclerosis.Atherosclerosis is a form of arteriosclerosis.

28. Lipoproteins classificationLipoproteins classification
 ChylomicronsChylomicrons - carry triacylglycerol (fat) from the- carry triacylglycerol (fat) from the
intestines to the liver and to adipose tissue.intestines to the liver and to adipose tissue.
 Very low density lipoproteinsVery low density lipoproteins - carry (newly- carry (newly
synthesised) triacylglycerol from the liver to adiposesynthesised) triacylglycerol from the liver to adipose
tissue.tissue.
 Low density lipoproteinsLow density lipoproteins - carry cholesterol from- carry cholesterol from
the liver to cells of the body ("bad cholesterol“).the liver to cells of the body ("bad cholesterol“).
 High density lipoproteinsHigh density lipoproteins - collects cholesterol from- collects cholesterol from
the body's tissues, and brings it back to the liverthe body's tissues, and brings it back to the liver
("good cholesterol“).("good cholesterol“).
ProteinFat

29. Atherosclerosis pathogenesisAtherosclerosis pathogenesis
The lipid hypothesis
plasma LDL penetration into the arterial wall  lipid accumulation in
smooth muscle cells and in macrophages (foam cells) smooth
muscle cell hyperplasia and migration into the subintimal and intimal
region

30. Atherosclerosis pathogenesisAtherosclerosis pathogenesis
The chronic endothelial injury hypothesisThe chronic endothelial injury hypothesis
Endothelial injuryEndothelial injury
loss of endothelium,loss of endothelium,
adhesion of platelets to subendothelium,adhesion of platelets to subendothelium,
aggregation of platelets,aggregation of platelets,
chemotaxis of monocytes and T-cell lymphocyteschemotaxis of monocytes and T-cell lymphocytes
release of growth factorsrelease of growth factors
induce migration and replicationinduce migration and replication
their synthesis of connective tissue and proteoglycanstheir synthesis of connective tissue and proteoglycans

31. AtherosclerosisAtherosclerosis
pathogenesispathogenesis
 The atherosclerotic plaque mayThe atherosclerotic plaque may
produce a severe stenosis or mayproduce a severe stenosis or may
progress to total arterial occlusion.progress to total arterial occlusion.
 With time, the plaque becomesWith time, the plaque becomes
calcified.calcified.
 Some plaques are stableSome plaques are stable
 Others may undergo spontaneousOthers may undergo spontaneous
fissure or rupture (unstable orfissure or rupture (unstable or
vulnerable)vulnerable)
 The ruptured plaque stimulatesThe ruptured plaque stimulates
thrombosis.thrombosis.

32. Atherosclerosis: positive riskAtherosclerosis: positive risk
factorsfactors
Non modifiableNon modifiable
 Age – middle to late.Age – middle to late.
 Sex – Males,Sex – Males,
complicationscomplications
 Genetic – FamiliarGenetic – Familiar
HypercholesterolemiaHypercholesterolemia
 Family history.Family history.
Potentially ModifiablePotentially Modifiable
 Hyperlipidemia –Hyperlipidemia –
HDL/LDL ratio.HDL/LDL ratio.
 Hypertension.Hypertension.
 Smoking.Smoking.
 DiabetesDiabetes
 Life style, diet, exerciseLife style, diet, exercise

33. Atherosclerosis risk factorsAtherosclerosis risk factors
 Negative risk factorsNegative risk factors
 high levels of circulating high density lipoproteinshigh levels of circulating high density lipoproteins
 moderate alcohol consumptionmoderate alcohol consumption
 cardiovascular fitnesscardiovascular fitness

34. Atherosclerosis symptomsAtherosclerosis symptoms
If the narrowing of an artery is less than 70% -If the narrowing of an artery is less than 70% -
asymptomaticasymptomatic
Symptoms occur due to the location of the narrowingSymptoms occur due to the location of the narrowing
 Coronary arteries – angina pectoris, heart attackCoronary arteries – angina pectoris, heart attack
 Carotid arteries - brain stroke.Carotid arteries - brain stroke.
 Arteries in the legs - leg cramps (intermittentArteries in the legs - leg cramps (intermittent
claudication).claudication).
 Renal arteries - kidney failure or high blood pressureRenal arteries - kidney failure or high blood pressure
(malignant hypertension).(malignant hypertension).

35. Atherosclerosis symptomsAtherosclerosis symptoms
 Symptoms occur due to deprivation of tissuesSymptoms occur due to deprivation of tissues
blood supplyblood supply
 The first symptom may be pain or cramps.The first symptom may be pain or cramps.
 Typically, symptoms develop gradually as theTypically, symptoms develop gradually as the
atheroma slowly narrows an artery.atheroma slowly narrows an artery.

36. Prevention and TreatmentPrevention and Treatment
Prevention – to modify risk factorsPrevention – to modify risk factors
 smoking,smoking,
 high blood cholesterol levels,high blood cholesterol levels,
 high blood pressure,high blood pressure,
 obesity,obesity,
 physical inactivity.physical inactivity.
 When atherosclerosis becomes severe theWhen atherosclerosis becomes severe the
complications themselves must be treated.complications themselves must be treated.