This document summarizes drugs used to manage hypotension and hypertension. It discusses drugs that can be used to treat hypotension like norepinephrine, phenylephrine, and methoxamine, which are direct-acting alpha agonists that increase blood pressure by constricting blood vessels. It also discusses various classes of drugs to treat hypertension, including ACE inhibitors, ARBs, calcium channel blockers, diuretics, and vasodilators. Each drug class is explained in terms of its mechanism of action and examples are provided of commonly used drugs within each class. Adverse effects are also outlined for each drug class.

1. Drugs for the management of hypotension &
hypertension

2. Introduction
Hypotension:
•BP below 100 / 60 mm Hg in women and less than 110 / 70
mm Hg in men.
•orthostatic hypotension (orthostasis = standing upright), the
blood rushes into the lower parts of the body when sitting down
or standing up fast.

3. Diseases :
•Severe hemorrhage
•Heart diseases (cardiac insufficiency, arrhythmias, pericarditis)
•Neurologic diseases
•Addison’s disease
Drugs
•Antihypertensive drugs
•Diuretics
•Anti-anginal drugs
•Vasodilators
•Antiarrhythmic drugs
•Antidepressants

4. Drugs used to treat hypotension
If cerebral, renal, and cardiac perfusion is maintained,
hypotension itself does not usually require vigorous direct
treatment
Sympathomimetic agents
Used in a hypotensive emergency to preserve cerebral &
coronary blood flow. The treatment is usually of short duration
while the appropriate intravenous fluid or blood is being
administered.
Direct-acting α agonists
• Norepinephrine,
• Phenylephrine, & Methoxamine

5. Direct-acting α agonists
Norepinephrine (Noradrenaline) is an agonist at
•both α 1, α 2, & β 1 receptors.
•↑peripheral resistance = ↑diastolic & systolic BP.
Phenylephrine pure α 1 agonist.
•longer duration of action than the catecholamines.
•↑peripheral resistance = ↑diastolic & systolic BP.
Methoxamine α 1 -receptor agonist.
• prolonged duration of action
•vagally mediated bradycardia.

6. Shock
• Complex acute cardiovascular syndrome that results in a
critical ↓ in perfusion of vital tissues & a wide range of
systemic effects.
• Usually associated with hypotension, an altered mental state,
oliguria, & metabolic acidosis.
• If untreated, it progresses to a refractory deteriorating state &
death.
Mechanisms responsible for shock :
• Hypovolemia, cardiac insufficiency, & altered vascular
resistance.
Volume replacement & treatment of the underlying disease are
the mainstays of the treatment of shock.

7. Shock
Cardiogenic shock and acute heart failure, usually due to
massive myocardial infarction, has a poor prognosis.
•Dopamine or dobutamine : positive inotropic drugs
•Dopamine acts on
β1 receptors ( cardiac stimulation)
dopaminergic receptors (renal & mesenteric vasodilation)
α1 receptors (vasoconstriction)
•Dobutamine acts on β1 ( cardiac stimulation)

8. Shock
Anaphylactic shock :
•Type I hypersensitivity reaction that affects both the respiratory
& the cardiovascular systems causing
•bronchospasm, mucous membrane congestion, angioedema, and
severe hypotension
•Inj Adrenaline, 0.3–0.5 mg IM
•Activates α, β1, and β2 receptors, all of which may be important
in reversing the pathophysiologic processes underlying
anaphylaxis
•Glucocorticoids and antihistamines (both H 1 - and H 2
-receptor antagonists) may be useful as secondary therapy in
anaphylaxis.

9. Introduction
Hypertension is the most common cardiovascular disease.
Sustained hypertension damages blood vessels in kidney, heart,
& brain and leads to an ↑incidence of renal failure, coronary
disease, cardiac failure, and stroke.
Normal Blood Pressure : Systolic 120 -129 mm Hg
Diastolic 80 – 84 ,,,,,,,,,,,
Mild Hypertension : 140 -159/90-99 ,,,,,,,,,,,,
Moderate Hypertension 160 -179/100-109 ,,,,,,,,,,
Severe Hypertension : >180/>110 ,,,,,,,,,,,

10. Introduction - III
Etiology:
• > 90% Unknown – Essential Hypertension ( so called because
it was originally thought the raised BP was essential to
maintain adequate tissue perfusion)
• Secondary to known organic diseases such as Renovascular
disease, Coarctation of aorta, Pheochromocytoma, Cushing’s
disease, Hyperaldosteronism, etc.
– The therapy is directed towards correction of underlying disease.
Risk factors:
• Smoking, Hyperlipidaemia, Diabetes mellitus, Obesity &
history of any cardiovascular disease.

11. Antihypertensive agents
1. Centrally acting sympathoplegics
2. Adrenoceptor Antagonists
α adrenergic receptor blockers
β adrenergic receptor blockers
3. Angiotensin Inhibitors
Angiotensin Converting Enzyme Inhibitors
Angiotensin Receptor Blockers
4. Calcium channel Blockers
5. Diuretics
6. Vasodilators

12. Centrally Acting Sympathoplegic Drugs
METHYLDOPA
Stimulates α2 receptors in vasomotor center (VMC) thereby
↓sympathetic outflow from CNS & thus ↓ Peripheral vascular
resistance, HR & CO.
Uses : Hypertension in Pregnancy & Mild-moderate hypertension
Adv effects:
Sedation, Hyperprolactinemia, Hemolytic anemia,
CLONIDINE
Stimulates α2 receptors in VMC, ↓sympathetic outflow & thus
↓ Peripheral vascular resistance, HR & CO.
Uses: Mild to moderate hypertension
Adv effects: Sedation, dry mouth, mental depression

13. α Adrenergic Blockers
PRAZOSIN: Doxazosin, Terazosin,
Mechanism of Action
• Blocks α1 receptors in arterioles & venules thereby produce
vasodilation, ↓ peripheral vascular resistance.
Uses : Mild to moderate hypertension,
Benign Prostate Enlargement,
Raynaud’s phenomenon,
Pheochromocytoma (Nonselective α blocker
Phenoxybenzamine)
Adv effects: Postural hypotension - Ist dose phenomenon
(Ist dose should be small & should be administered at bed time).
Nasal stuffiness, dizziness, palpitation.

14. βAdrenergic Blockers
Cardioselective (β1 Selective): Atenolol, Metoprolol, Bisoprolol,
Nonselective (β1 & β2 ): Propranolol, Nadolol, Carteolol.
α & β Blockers: Labetalol, Carvedilol
Mechanism of Action:
• Block β1 receptors in heart, ↓HR & CO
• Inhibit β1 mediated Renin secretion from Juxtaglomerular
cells (kidney) thereby depress the Renin-angiotensin-
aldosterone system causing vasodilation & ↓ sodium & water
retention.
Adv effects: Bradycardia, bronchoconstriction (worsening of pre
existing asthma), cold clammy skin, fatigue, impotency, mask
the hypoglycemic symptoms in Type 1 DM

16. ACE inhibitors
Captopril, Enalapril, Lisinopril
• By inhibiting ACE they ↓formation of Angiotensin II, thereby
causing vasodilation, ↓Na & water retention & inhibit
Bradykinin metabolism thus ↑ vasodilation.
Uses:
Hypertension, Chronic Heart Failure & Diabetic nephropathy
Adv effects:
Dry cough, Angioedema, Hypotension Hyperkalemia,
Teratogenicity ( Fetal hypotension, anuria & renal failure)

17. Angiotension receptor blockers (ARBs)
Losartan, Valsartan, Olmisartan, Telmisartan,etc
• Block the action of Angiotensin II on AT1 receptors =>
Vasodilation &
• Inhibit Aldosterone secretion => ↓Na & water retention thus ↓
BP
Advantages:
Do not inhibit Bradykinin & hence no dry cough, angioedema
& bronchospasm
Contraindications of ACE-Inhibitors & ARBs:
• Pregnancy
• Patients with renal artery stenosis

18. Calcium channel blockers
Amlodipine, Nifedipine, Nimodipine,
Mech of action
Block the L-type calcium channels in the arterial smooth muscles
=> Inhibition of calcium influx & Relaxation of smooth
mucles => Vasodilation & ↓ BP
Uses : Mild to Moderate Hypertension
Subarachnoid hemorrhage (Nimodipine),
Adv effects:
Reflex tachycardia, Headache, Flushing, Constipation,
Peripheral edema,

19. Thiazide Diuretics
MOA:
• Inhibit NaCl reabsorption by blocking Na+/Cl- tranporter in distal
convulated tubules => Natriuresis => ↓ Blood volume & ↓ BP
Uses:
• Mild to Moderate Hypertension
• Chronic Heart Failure
Adverse effects
• Hypokalemia, Hyperuricemia , Hyperglycemia , Hyperlipidemia
• Hyponatremia

20. Loop Diuretics
MOA:
• Inhibit Na/K/2 Cl cotransporter in the Thick limb of ascending
loop of Henle. => Natriuresis => ↓ Blood volume & ↓ BP
Uses:
• Moderate, Severe & Malignant Hypertension
Adverse effects
• Hypokalemia
• Ototoxicity
• Hyperuricemia
• Hyponatremia

21. VASODILATORS
Relax vascular smooth muscles => ↓Peripheral vascular resistance
Oral : Hydralazine & Minoxidil
Parenteral : Sodium Nitroprusside, Diazoxide
HYDRALAZINE
Arteriolar vasodilation, ↓Peripheral vascular resistance ↓BP
Metabolized by Acetylation – genetically determined.
Rapid acetylators have greater first pass metabolism, ↓ bioavailability
& less antihypertensive benefit than do slow acetylators.
Uses : Mild to Moderate hypertension
Adv effects: Reflex tachycardia, Palpitation, Headache, Lupus
erythematosus ( arthralgia, myalgia, skin rashes, & fever),
Peripheral neuropathy.

22. VASODILATORS
Uses of Sodium Nitroprusside:
Hypertensive emergencies, Severe heart failure
Adv effects: Accumulation of Cyanide ( metabolic acidosis,
arrhythmias, excessive hypotension),
Thiocyanate toxicity ( Weakness, Disorientation, Psychosis,
& Convulsions), Hypothyroidism, Methemoglobinemia
DIAZOXIDE
Long acting parenteral arteriolar vasodilator, acts by opening
potassium channels in vascular smooth muscles thereby ↓
peripheral vascular resistance & thus ↓BP
Uses : Hypertensive emergencies
Adverse effects; Excessive hypotension, Reflex tachycardia,
Hyperglycemia