Cology
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NAME :- JIBAN PRASAD KUNDU
ROLL NO :- 20101922050
GROUP :- A2
SEM :- 5th
SUBJECT :- PHARMACOLOGY II
SUBJECT CODE :- PT518
TOPIC :- SUMERIZATION ON HYPERTENSION AND IT’S TREATMENT
HYPERTENSION
INTRODUCTION:-
Hypertension, also known as high blood pressure, is a long-term
medical condition in which the blood pressure in the arteries is
persistently elevated.High blood pressure usually does not cause
symptoms itself.It is, however, a major risk factor for stroke,
coronary artery disease, heart failure, atrial fibrillation,
peripheral arterial disease, vision loss, chronic kidney disease, and
dementia. Hypertension is a major cause of premature death
worldwide.
As per Joint National Committee (JNC) guidelines on hypertension pressure is graded as:-
CLASSIFICATION SYSTOLIC (mm hg) DIASTOLIC (mm hg)
Normal <120 <80
Pre-hypertension 120-139 80-89
Stage I 140-159 90-99
Stage II >160 >100
Blood pressure is determined by cardiac output (CO) and total
peripheral vascular resistance (PVR).
Blood pressure is controlled by baroreceptor reflexes acting
through along with renin angiotensin-aldosterone system.
Types of hypertension
Primary (Essential) Hypertension
Definition:-This is the most common type of hypertension, accounting for about 90-95% of
cases. It develops over time without a specific identifiable cause.
Causes:-Often linked to genetic factors, lifestyle (e.g., poor diet, lack of exercise), and age.
Secondary Hypertension
Definition:-This type of hypertension is caused by an underlying condition or disease.
Causes:-Kidney disease, hormonal disorders (e.g., hyperthyroidism), certain medications,
sleep apnea, or tumors.
There are some other type of hypertension which are Isolated Systolic
Hypertension, Malignant Hypertension , Resistant Hypertension,
White Coat Hypertension, Masked Hypertension, Pulmonary
Hypertension
CAUSES OF HYPERTENSION
1. Underlying health conditions
2. Overweight or obesity
3. Lack of physical activity
4. Salt intake
5. Alcohol
6. Caffeine
7. Smoking
8. Medication
9. Not enough sleep
10.Pregnancy
11.Age
12.Genetics
Treatment of hypertension
Mechanism of Action of RAAS Inhibitors in Hypertension
ACE Inhibitors (Angiotensin-Converting Enzyme Inhibitors)
Mechanism:-ACE inhibitors block the enzyme ACE, preventing the conversion of angiotensin I
to angiotensin II.
Renin Inhibitors
Mechanism: Renin inhibitors directly inhibit renin, the enzyme that starts the RAAS cascade by
converting angiotensinogen to angiotensin I.
ARBs (Angiotensin II Receptor Blockers)
Mechanism: ARBs block the angiotensin II receptors (specifically the AT1 receptor) on blood
vessels and other tissues.
Diuretics Mechanisms of Action
•Mechanism:-Thiazide diuretics inhibit the sodium-chloride symporter in the distal convoluted
tubule,
reducing the reabsorption of sodium and chloride from the filtrate back into the bloodstream.
•This leads to an increase in the excretion of sodium and water in the urine, reducing blood volume.
•By decreasing blood volume, these diuretics reduce cardiac output (the amount of blood pumped
by
the heart) and, over time, reduce peripheral vascular resistance, which lowers blood pressure.
Calcium channel blockers (CCBs)
Mechanism of Action:-
Calcium channel blockers inhibit the movement of calcium ions through L-type calcium
channels, which
are found in the smooth muscle cells of blood vessels, cardiac myocytes (heart muscle cells),
and pacemaker cells (cells that control heart rhythm).
Vasodilators
Mechanism of Action:-
Direct Smooth Muscle Relaxation
It is thought to work by interfering with calcium release from the sarcoplasmic reticulum in
smooth muscle cells, reducing calcium's ability to cause contraction, and thus leading to
vasodilation.
Sympathetic Inhibitors
Alpha-Adrenergic Blockers (Alpha Blockers)
Mechanism of action:-
Alpha blockers selectively block alpha-1 adrenergic receptors located on
the smooth muscle of blood vessels.
•Norepinephrine, a neurotransmitter released by sympathetic nerve endings,
normally
binds to these receptors, causing vasoconstriction (narrowing of blood
vessels).
•By blocking these receptors, alpha blockers prevent norepinephrine from
exerting its vasoconstrictive effects, leading to vasodilation (widening of
blood vessels).
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