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Anti-hypertensive drugs
1. Dhaka International UniversityDhaka International University
Department of PharmacyDepartment of Pharmacy
A Presentation onA Presentation on
Antihypertensive DrugAntihypertensive Drug
Presented By:Presented By:
Al imranAl imran
B.pharm.B.pharm.
2. What is hypertention?
WHO standard:WHO standard:
Hypertension:Hypertension: People whose blood pressure isPeople whose blood pressure is
elevated to More than 140/90mmHg requireelevated to More than 140/90mmHg require
antihypertensive agents.antihypertensive agents.
The diagnosis ofThe diagnosis of hypertensionhypertension is based on repeated,is based on repeated,
reproducible measurements of elevated blood pressure.reproducible measurements of elevated blood pressure.
4. Normal Systolic Blood Pressure
90—140 mmHg
Normal Diastolic Blood Pressure
60—90 mmHg
5.
6. Normal Regulation of Blood
Pressure :-
Arterial blood pressure (BP) is directly
proportionate to the product of the blood
flow (cardiac output(CO)) and the
resistance to passage of blood through
precapillary arterioles (peripheral
vascular resistance(PVR)):
BP = CO X PVR
7. Normal regulation of Blood Pressure
Blood pressure is maintained by
moment to moment regulation of
CO and PVR
Exerted at 4 anatomic sites
(arterioles, post capillary venules,
kidney and heart)
Baroreflexes mediated by
autonomic nerves, act in
combination with humoral
mechanisms to coordinate
functions of these 4
Maintain normal blood pressure
8. Normal regulation of blood pressure
(Postural Baroreflex)
Increased BP stretches the carotid arteries &aorta causing the
baroreceptors to increase their basal rate of action potential
generation.
Action potentials are conducted by the glossopharngeal &
vagus nerves to the cardioregulatory & vasomotor centers in
the medulla oblongata.
As a result of increased stimulation from the baroreceptors,
the cardio regulatory center increases parasympathetic
stimulation to the heart, which decreases the heart rate.
9. Normal regulation of blood pressure
(Postural Baroreflex)
Also decreases sympathetic stimulation to the heart which
decreases heart rate & stroke volume.
The vasomotor center decreases sympathetic stimulation to
blood vessels causing vasodilation which elevated BP back
toward normal.
13. Beta –Adrenoceptor-Blocking Agent/Beta
Blockers(Propranolol)
It was the first beta blocker shown to effective in
hypertension and ischemic heart disease.
It is a non selective beta blocker.
Now it is largely replaced by cardioselective beta
blockers (Metoprolol & Atenolol).
They are useful for lowing BP in mild to moderate
hypertension.
15. Beta –Adrenoceptor-Blocking Agent/Beta
Blockers(Metoprolol &Atenolol)
They are Beta-1 selective blocker.
Block Beta-1 receptors.
Prevent sympathetic cardiac stimulation .
Reduce renin secretion.
Used in hypertension and heart failure.
16. Vasodilators (Hydralazine, Minoxidil)
This class of drugs includes the oral vasodilators.
Which are used for long term outpatient therapy of
hypertension.
Parenteral vasodilators (nitroprusside,diazoxide) are
used to treat hypertension emergencies.
20. Mechanism & Sites of Action :
Renin release from the kidney cortex is stimulated by reduced renal
arterial pressure, sympathetic neural stimulation, and reduced
sodium delivery.
Renin acts upon angiotensinogen to split off the inactive precursor
decapeptide angiotensin I.
Angiotensin I is then converted, primarily by
Endothelial ACE, to the arterial vasoconstrictor octapeptide
angiotensin II ,which is in turn converted in the adrenal gland to
angiotensin III.
21. Angiotensin II has vasoconstrictor and
sodium-retaining activity.
Angiotensin II and III both stimulate
aldosterone release.
Two classes of drugs act specifically on the
renin-angiotensin system: the ACE
inhibitors and the competitive inhibitors of
angiotensin at its receptors
25. Captopril
Inhibit the converting enzyme angiotensin I to
angiotensin II .
Inhibit the inactivation of Bradykinin, a potent
vasodilator, which works at least in part by stimulating
release of nitric oxide and prostacyclin.
Hypotensive activity of Captopril results both from an
inhibitory action on the renin-angiotensin system
and a stimulating action on the kallikrein-kinin
system
26. Enalapril
Is a prodrug that is converted by
deesterification to a converting enzyme
inhibitor, Enalaprilat, with effects similar
to captopril.
Available only for intravenous use,
Use : primarily for hypertensive
emergencies.
27. Lisinopril is a lysine derivative of enalaprilat.
Benazepril, fosinopril, moexipril, perindopril,
quinapril, ramipril, and trandolapril are other
long-acting members of the class.
All are prodrugs, like enalapril, and are
converted to the active agents by hydrolysis,
primarily in the liver.
28. Angiotensin II inhibitors lower blood
pressure principally by decreasing
peripheral vascular resistance.
Cardiac output and heart rate are not
significantly changed.
Useful role in treating patients with diabetic
nephropathy because they diminish
proteinuria and stabilize renal function.
29. Indication of ACE Inhibitors:
Hypertension
Congestive heart failure (CHF)
Left ventricular dysfunction
Prevention of nephropathy in diabetes
mellitus
Following myocardial infarction.
30. All converting enzyme inhibitors are contraindicated
in patients with bilateral renal artery disease or with
unilateral renal artery disease and one kidney.
The inhibition of circulating RAS is major mechanism of antihypertensiv actyion of ACEIs. However only the acute Antuhypertensive effects correlate with the degree oif inhibition of circulating converting enzyme. After chronic administration, although antihypertensive effects is still present, there is not corelation with inhibition of plasma ACE, evenmore, there is a partial “escape” of ACE inhibition, and there are also increased plasma concetration of ACE. This is probably due top induction of ACE production, by it chronic inhibition. For the chronic antihypertensive effects it seems that more important is the inhibition of tissue ACE. next possible mechanisms is the inhibition of sympathetic activity. Ang II increases NE release from Sy nerve endings, enhance the sympathetic tone by central mechanuism, and by faciliotation of ganglionic transmission. In addition Ang II postsynaptic vasoconstrictor responce mediated by alfa-1 receptors.