Hta

2. PATHOPHYSIOLOGY OF
HYPERTENSION

3. PATHOGENESIS

4. • Peripheral autoregulatory
components
• Baroreceptor reflex
Neuronal
mechanisms
• Renin angiotensin
aldosterone pathway {
RAAS}
• Natriuritic hormone
Humoral
mechanism
• Electrolytes and chemicals
• Vascular endothelial
mechanisms
Other
mechanisms

5. HUMORAL MECHANISMS
 RAAS PATHWAY
 endogeneous system
 Activation and regulation is goverened by kidney.
 RAAS regulates sodium
potassium
fluid balance
This influences vascular tone and sympathetic
system activity.
Also plays a important role in regulation of BP.

6. RENIN IS STORED IN JUXTA
GLOMERULAR CELLS
 RENIN RELEASED DURING THESE FACTORS:-
• Perfusion pressure
• catecholamines
• Angiotensin ii
Intrarenal
factors
• Sodium,pottasium
• calcium
Extrarenal
factors

7. THE FACTORS THAT STIMULATE RENIN
SECRETION
Stimulate
renin
secretion
Decreased
sodium,potas
sium and
calcium
levels
Decreased
renal
pressure and
kidney blood
flow
catacholamin
es

8.  Renin catalyses angiotensinogen
angiotensin I
angiotensin converting
enzyme
angiotensin ii
after binding to specific
receptors AT1 and AT2
it exerts its effect

10. HOW ANGIOTENSIN II CAUSE INCREASE IN
BLOOD PRESSURE ?
Angiotensin ii stimulate
Aldosterone
synthesis from
cortex
Sodium, water
reabsorption
Increase in
plasma
volume,peripheral
resistance ,BP

11. LOCAL RAAS SYSTEM
IN HEART
• Angiotensin ii is
generated from
angiotensin
convertase
enzyme
• Activation of
RAAS causes
myocardial
contractability
In BRAIN angio ii
modulates release
of pituitary
hormones and
enhances
sympathetic
outflow from
medulla oblongota
In PERIPHERAL
TISSUES
Generate
angiotensin
peptides and
cause increase in
vascular
resistance

12. NATRIURETIC HORMONE
increase in
concentration of
natriuretic hormone
Inhibits sodium
potassium ATP ase
pump
Inhibition of sodium
transport across the cell
membrane
Increase in vascular
tone and BP

13. NEURONAL MECHANISM
 Central and autonomic nervous system involved in
the regulation of BP.
 Number of receptors are present either enhance or
inhibit the release of nor epinephrine and are
located in the presynaptic terminal.
 Stimulation of presynaptic terminal:-
 Alpha 1- exerts negative inhibition on release of nor
epinephrine
 Beta-facilitate release of nor epinephrine

14.  Stimulation of postsynaptic terminal

15. BARORECEPTOR REFLEX
 Major negative feedback mechanism.
 Controls symphathetic activity
 Present on nerve endings lying on walls of large
artery eg:- carotid artery.
 Alpha 2 adrenergic stimulation causes decrease in
BP through vasomotor area.
 Angiotensin ii cause increase in symphathetic
outflow and result in increase in BP.
 Stimulation of nucleus tractus
solitaries,vasomotor area etc cause increase or
decrease in BP.

16. BARORECEPTOR REFLEX

17.  PERIPHERAL AUTOREGULATORY COMPONENTS
Kidneys maintain normal BP
volume pressure adaptive mechanism

18. LOCAL AUTOREGULATORY PROCESS–
MAINTAINS TISSUE OXYGENATION
IT IS ACTIVATED TO OFFSET INCREASED BLOOD
FLOW.
When tissue o2
demand
decreases
Increase in
metabolic
demand
Trigger the
arteriolar
vasodilation
That lowers
peripheral
resistance
Cause increased
blood flow and
oxygenation

19. VASCULAR ENDOTHELIAL MECHANISMS
 Deficiency of vasodilating substances like
{bradykinin,prostacyclin} and increase in
vasoconstricting substances like{angiotensin
ii,endothelin i} cause artherosclerosis and
hypertension.
Nitric
oxide
Potent vasodilator
Relaxes vascular epithelium
Regulator of arterial BP

20. ELECTROLYTES AND CHEMICALS
 calcium depletion

21. ELEVATED URIC ACID LEVEL AND POTASSIUM
DEPLETION
Pottasium
depletion
cause
Increased
peripheral
vascular
resistance
Increased BP

22. HOW INSULIN INCREASES BP?
 Increased insulin concentration lead to
hypertension because increased renal sodium
retention and enhanced sympathetic activity
 Insulin elevate BP by increasing calcium levels
which leads to increased vascular resistance

23. COMPLICTIONS IN HYPERTENSION PATIENTS
 Elevated BP
 Obesity
 Dyslipidemia
 Elevated blood glucose