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Hypertension.pptx
1. Hypertension
presented by:
Mr. Sanjoy chungkrang
Lecturer, Department of Pharmaceutical science
Northeast Frontier Technical University, Alo, Arunachal Pradesh
2. Introduction:
• Hypertension is defined as blood pressure above 140/90 on three consecutive
measurements at least 6 hours apart.
• Consistently high BP causes the heart to work harder than it should and can
damage the coronary arteries, the kidneys, the brain, and the eyes.
• Hypertension is major cause of STROKE.
3. • Normal - <120/80
• Pre-hypertension – 120-139/80-89
• Hypertension –
• Stage 1 – 140-159/ 90-99
• Stage 2 - ≥ 160/ ≥ 100
RANGE OF BLOOD PRESSURE
4. Types:
Primary hypertension Secondary hypertension
• Specific cause unknown.
• 90% of the cases.
• May due to stress, obesity, smoking,
more Na+ intake, insomnia and life style.
• Cause is known (Renal artery disease,
pregnancy etc.)
• 10% of the cases.
5. ANTI- HYPERTENSIVES
• These are the drugs/Agents which are used in the treatment of
hypertension.
• Following categories can be given as single or in combinations
based on patient condition.
7. 1. ACE Inhibitors
• Captopril, Enalapril, Lisinopril, Ramipril, Etc.
• These are the first choice of drugs in the treatment of hypertension
renal artery stenosis & Renal disease where excessive levels of renin
are released, causing high levels of angiotensin ( a potent
vasoconstrictor ) and aldosterone.
• ACE inhibitors lower circulating angiotensin II and increase
Bradykinin, a potent vasodilator.
8. Mechanism Of Action
Angiotensinogen
RENIN
renal arterial pressure
renal sympathetic
nerve activity
Vasoconstrictor
Na+ in renal tubular
fluid
Angiotensin-I
Angiotensin-II
X ACE
Na+ & H20 retention
B P Blood volume
9. Pharmacokinetics:
• Well oral absorption
• half life is 11-12 hours.
• Primary eliminated by kidney than bile and faces
• Care should be taken if given to patient with liver and kidney
failure
• Adverse effects:
• Dry cough (dur to bradykinins)
• Hyperkalemia
• Angioedema
• Loss of taste sensation
• Tachycardia, pulpitation
10. 2. Angiotensin Receptor Antagonist
• Losartan -- it’s a competitive antagonist of Angiotensin II.
• It blocks all the action of Angiotensin II like vasoconstriction
etc
• MOA:
Angiotensin
e-II Effects
3. Release of
adrenaline
4. Central and peripheral
stimulation
1. Vasoconstriction
2. Release of
Aldosterone
11. Pharmacokinetics:
• Well oral absorption
• Losartan –Dose – 50 mg /day
• Metabolized in liver and excreted out by kidney
• Additionally 12.5 mg/day hydrochlorthiazide can be given to
enhance the overall action.
• comparatively safe – do not cause increase in bradykinin levels
• Adverse effects:
• No side effects
• Rarely - Angioedema
• Loss of taste sensation and urticaria
13. MOA
• Causes smooth muscles relaxation by blocking the binding of Ca+ to its
receptor – preventing muscle contraction
• This causes decreased in peripheral smooth muscles tone and
decreased systemic vascular resistance
Decreased blood pressure
14. Pharmacokinetic
s:
• 90–100% absorbed orally, peak occurring at 1–3 hr (except amlodipine 6–9
hr).
• The oral bioavailability of ca2+ channel blockers is incomplete with
marked inter- and intraindividual variations due to high first pass
metabolism
• All are highly plasma protein bound (min.: Diltiazem 80%, max.:
Felodipine 99%).
• High clearance drugs with extensive tissue distribution.
• > 90% metabolized in liver and excreted in urine.
• The elimination t½ are in the range of 2–6 hr.
• Adverse effects:
• Headache, constipation, rash, nausea, flushing, edema (fluid accumulation in tissues), drowsiness.
15. Uses/indications:
1) Hypertension
2) Angina Pactoris
3) Cardiac Arrhythmias
4) • Congestive Heart Failure
5) • Myocardial Infraction
6) • Alopecia
7) • Bronchial Asthma
8) • Urinary Urge Incontinence
9) Other Uses- Nifedipine Is An Alternative Drug For
Premature Labour, Erectile Dysfunction
17. 4. Diuretics
• Hydrochlorothiazide, Indapamide Furosemide, Amiloride
• Diuretics Have Been The Standard Antihypertensive Drugs
Over The Past 4 Decades, Though They Directly Don’t
Decrease BP.
18. • Decrease the plasma and extracellular fluid volumes/ Blood volume
• Results: decreased preload
decreased cardiac output
decreased total peripheral resistance
• Overall effect: decreased workload of the heart,
and decreased blood pressure
MOA:
19. SIDE EFFECTS
• Low sodium in your blood (hyponatremia)
• Dizziness.
• Headaches.
• Dehydration.
• Muscle cramps.
• Joint disorders (gout)
• Impotence
20. 5. ALFA- Adrenergic Blockers
• Prazosin, Terazosin, Doxazosin, Phentolamine, Phenoxybenzamine
• They Are Mild Anti Hypertensives. Used for stage 1 otherwise given as a combination with
other drugs.
• Prazosin :This Prototype Selective Α1 Antagonist Dilates Both Resistance Vessels. There Is
Little Reflex Cardiac Stimulation And Renin Release During Long-term Therapy
• Postural Hypotension And Fainting May Occur In The Beginning—called ‘First Dose Effect’,
And With Dose Increments. This Disappears With Continued Therapy, But May Persist In
The Elderly. For This Reason, Prazosin Is Always Started At Low Dose (0.5 Mg) Given At
Bedtime And Gradually Increased With Twice Daily Administration Till An Adequate
Response Is Produced (Max. Dose 10 Mg BD).
21. Side effects:
• Prazosin Is Generally Well Tolerated At Low Doses. But Some Time
• Postural Hypotension
• Headache,
• Drowsiness, Dry Mouth,
• Weakness, Palpitation,
• Nasal Blockade, Blurred Vision And Rash.
• Ejaculation May Be Impaired In Males: Especially With Higher Doses.
• USES:
• PRazosin is a moderately potent antihypertensive with many desirable
features, but is noT Used as a first line drug because fluid retention and
tolerance gradually develops with monotherapy
22. 6. Beta Adrenergic Blocker
• They are mild antihypertensives; do not significantly lower BP in normotensives. Used
alone they suffice in 30–40% patients—mostly mild to moderate cases. In the large
majority of the rest, they can be usefully combined with other drugs.
• The hypotensive response to β blockers develops over 1–3 weeks and is well sustained.
• Despite short and differing plasma half lives, the antihypertensive action of most β
blockers is maintain
• Because of absence of postural hypotension, bowel alteration, salt and water retention; a
low incidence of side effects, low cost; once a day regimen and cardioprotective potential,
23. 7. Central sympatholytics
• Clonidine, Methyldopa
• MoA: stimulate alfa 2 receptor of vasomotor center
• Central outflow increases
• Sympathetic outflow increases
• Increase in BP
These drugs inhibit
Given Pathway
24. Clonidin
e
• It is an imidazoline derivative having complex actions. Clonidine is a partial
agonist with high affinity and high intrinsic activity at α2 receptors, especially
α2a subtype in brainstem. The major haemodynamic effects result
• From stimulation of α2a receptors present mainly postjunctionally in medulla
(vasomotor centre)→ decrease sympathetic out flow → fall in BP and
bradycardia (also due to enhanced vagal tone). Plasma NA declines
• MOA: SAME
• Pharmacokinetics: Clonidine is well absorbed orally; peak occurs in 2–4 hours;
• 1/2 to 2/3 of an oral dose is excreted unchanged in urine, the rest as
metabolites.
• Plasma t½ is 8–12 hours.
• Effect of a single dose lasts for 6–24 hours.
25. Adverse
effects
• Sedation, mental depression, disturbed sleep; dryness of mouth, nose
and eyes (secretion is decreased by central action),
• Constipation (antisecretory effect on the intestines).
• Impotence, salt and water retention, bradycardia (due to reduced
sympathetic tone).
• Postural hypotension occurs, but is mostly asymptomatic.
• Alarming rise in bp, in excess of pretreatment level,
• With tachycardia, restlessness, anxiety, sweating
• Drug interactions: tricyclic antidepressants and chlorpromazine abolish the
antihypertensive action of clonidine, probably by blocking α receptors
on which clonidine acts.
27. Hydralazine
• It is a directly acting arteriolar vasodilator
• MOA: The mechanism of vascular smooth muscle relaxant action of hydralazine
is not clearly known. It is partly endothelium dependent: may involve
generation of NO (nitric oxide) and stimulation of cgmp. Direct effects on
membrane potential and on ca2+ fluxes have also been proposed.
• Pharmacokinetics: Hydralazine is well absorbed orally, and is subjected to first pass
metabolism in liver. The chief metabolic pathway is acetylation. there are slow
and fast acetylators. Bioavailability is higher in slow acetylators,
• Hydralazine is completely metabolized both in liver and plasma; the
metabolites are excreted in urine,
• t½ 1–2 hours. However, hypotensive effect lasts longer (12 hours), probably
because of its persistence in the vessel wall
28. Adverse effects
• Are frequent and mainly due to vasodilatation.
1. Facial flushing, conjunctival injection, throbbing, headache, dizziness, palpitation,
nasal stuffiness, fluid, retention, edema.
2. Angina and MI may be precipitated in patients with coronary artery disease.
3. Postural hypotension is not prominent because of little action on veins: venous
return and C.O. Are not reduced.
4. Paresthesias, tremor, muscle cramps.
• USES: Used in moderate-to-severe hypertension. It is not Used alone.
• Hydralazine can be used in patients with renal involvement, but is
contraindicated in older patients and in those with ischaemic heart disease.
• It is one of the preferred antihypertensives during pregnancy because of
decades of experience and record of safety.
29. • Minoxidil : it is a powerful vasodilator, the pattern of action resembling
hydralazine, i.E. Direct relaxation of arteriolar smooth muscle
• Minoxidil is a prodrug—converted to an active metabolite (by sulfate
conjugation) which is an opener of ATP operated K+ channels; acts by
hyperpolarizing smooth Muscle.
• Minoxidil is indicated only rarely in severe or life-threatening hypertension.
• Use in alopecia: minoxidil increases growth of body hair. Applied topically (2%
twice daily) it promotes hair growth in male pattern baldness and alopecia
areata.
• The response is slow (takes 2– 6 months) and incomplete, but upto 60%
subjects derive some benefit. Baldness recurs when therapy is discontinued.
The mechanism of increased hair growth is notKnown; may involve:
• (A) enhanced microcirculation around hair follicles.
• (B) direct stimulation of resting hair follicles.
• (C) alteration of androgen effect on genetically programmed hair follicles.