HYPERTENSION
DEFINITION
It is high blood
pressure. The pressure
exerted by blood on the
wall of systemic artery
is called blood pressure.
TYPES OF HYPERTENSION
Primary → Genetic, lifestyle, stress
Secondary → Due to disease
Malignant → Severe, diastolic rise, death possible
Gestational → During pregnancy
CAUSES OF HYPERTENSION
• Stress
• Age (>40)
• High Sodium (high salt)
• Lack of physical activity
• Habitat
• Obesity → Fat in vessels → High BP
OVERACTIVATION Activate SNS
OF SNS
Neurotransmitter
release
Constriction of blood
vessels
BP Rises
SODIUM WATER RETENTION
ANGIOTENSIN II REABSORPTION INCREASED BP RISES
RISES OF NA⁺ & H₂O BLOOD VOLUME
RAAS (RENIN ANGIOTENSIN ALDOSTERONE SYSTEM)
Renin Convert
Kidney Releases Liver
Low BP Angiotensinogen Angiotensin I
Renin (Angiotensinogen)
into Angiotensin I
Vasoconstriction
Blood Volume Na⁺ & H₂O
& Aldosterone Angiotensin II ACE (lungs)
Increases retention
release
BP Increases
CLASSIFICATION OF HYPERTENTION
Normal: 120/80
Pre-hypertension: 120–129 / 80–90
Stage I: 140–159 / 90–99
Stage II: ≥160 / ≥100
HYPERTENSION They continuously monitor the pressure of blood flow &
work according to the pressure of blood.
CONTROLLING
MECHANISMS: For few times they act by changing the activity of
sympathetic nervous system.
BARO
RECEPTORS Decrease Blood pressure it activates the Baro Receptor & it
leads to Increases the sympathetic system & decrease the
Parasympathetic system.
Increase in sympathetic system it leads to vasoconstriction
& it automatically increase the Cardiac output & it leads to
Increase in B.P.
Kidney provide the long term Control of B.P. by altering the blood
volume.
HYPERTENSION Decrease in B.P. It activates the Baro Receptor & It release the renin.
CONTROLLING
MECHANISMS: Low Sodium Intake Or high Sodium loss leads to release of Renin.
RENIN
ANGIOTENSIN
Renin converts Angiotensinogen into Angiotensin I.
ALDOSTERONE ACE Converts the Angiotensin I into Angiotensin II.
SYSTEM
Angiotensin II is a potent circulatory vasoconstrictor.
Angiotensin II Constricts arterioles and veins.
Angiotensin II stimulates the release of Aldosterone & It
causes/increases sodium reabsorption. & It leads to Increase the blood
volume & automatically B.P. Increases.
DIURETICS Thiazides diuretics
eg :- Hydrochlorthiazide
• It decreases the Na⁺ & H₂O retention. It leads to decrease in
blood volume & automatically cardiac output decreases.
• With long term use it decreases the total peripheral vascular
resistance (TPR) – in vessels resistance caused which resist the
flow of blood.
• Potassium sparing diuretics + Thiazides diuretics :- It decreases
the amount of Potassium loss. It can be combined with β –
blockers + ACE + Angiotensin receptor blockers.
Adverse effects of Thiazides diuretics :
• Hypokalemia
• Hyperurecemia
• Acute Gout
• Increase total & LDL cholesterol (bad cholesterol)
• Thiazides are more effective in elderly
• They show maximum antihypertensive activity in 25 mg / day
DIURETICS High ceiling / loop diuretics
(CONTD.)
eg :- Furosemide
Furosemide is strong diuretic but
weaker antihypertensive activity.
If there is fall in B.P. :- By decreasing
the plasma volume and cardiac output.
It can cause more electrolyte
imbalance.
ALDOSTERONE ANTAGONIST
Angiotensinogen
Renin (Kidney)
Angiotensin I
ACE (Lungs)
Angiotensin II
Stimulate
Blocks
Aldosterone Adrenal Cortex
Antagonist
Release
Aldosterone
RENIN ACE Inhibitors
ANGIOTENSIN
Eg.: Captopril, Enalpril, Ramapril
SYSTEM
(Liver) Angiotensinogen
Renin (Kidney)
INHIBITORS Angiotensin I
ACE Inhibitors Blocks ACE (Lungs)
Angiotensin II
Vasoconstriction
Increase B.P.
DIRECT RENIN It blocks the release of renin in kidney
INHIBITORS
Adverse Effects
1. Dry Cough
2. Rash
3. Fever, Altered the taste and hyperkalemia
ΒETA - BLOCKER • They are Sympathetic Inhibitors.
• Eg.: Atenolol, Metaprolol.
• β – blockers Lowers the BP by decreasing the release of
renin from kidney.
• They Decrease the formation of Angiotensin II they
decrease the secretion of Aldosterone.
• Non – selective β – blockers eg : Propranolol are not used
in Asthmatic patients due to the blockage of β₂ in lungs
because it cause the Bronchoconstriction
• α – blockers :- eg – Perazosin, Terazosin, Doxazosin,
Prazosin
MOA :-
It dilates the blood vessel
CENTRAL • Eg.: Clodidine Clonidine Clanicidine
• Lowers the sympathetic Nervous
SYMPATHOLYTIC system
CALCIUM Eg.: Verapamil, Diltiazem, Amlodipine
CHANNEL Types of Calcium Channel :
Voltage sensitive channel: It is activated when potential
BLOCKERS drops to -40 mV.
Receptor operated channel: It is activated by adrenaline in
case of fright.
Leak channels: These are small amount of calcium channels
& leak into resting cells & pumped out by calcium ATPase
Types of Voltage sensitive Ca²⁺ Channel:
(a) L – Type :- These are long lasting current. Mostly Ca⁺⁺ ion
channel work on L – type channel.
(b) T – type :- Transient current.
(c) N – type :- Neuronal current.
CALCIUM Mechanism Of Action:
CHANNEL Effect on smooth muscle – These dilates the
BLOCKERS vessels & remove or recover the pain.
(CONTD.) These Ca²⁺ channel blockers binds with the L
– type Ca²⁺ channel & prevent the entry of
Ca²⁺ into the cell.
It reduces the myocardial contraction & it
leads to decrease in heart rate & decrease
the force of contraction results in decrease
in myocardial workload.
They cause the dilation of vessels.
VASODILATORS Examples: Hydralazine, Minoxidil
Minoxidil: Do not use in 1st preference for
vasodilators. It causes excessive growth of hair in
face of women.
Mechanism of Action:
It produces the relaxation of vascular smooth
VASODILATORS muscles.
(CONTD.) They activate the K⁺ channel & increase the K⁺
efflux.
Rise in K⁺ efflux leads to hyperpolarization of
smooth muscles.
If membrane is hyperpolarized, it will decrease the
Ca²⁺ influx.
If Ca²⁺ influx is decreased, then it leads to arteriolar
relaxation.
Other actions of vasodilators:
They may cause angina & myocardial infarction.
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