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  • Hypertension is the most common cardiovascular disease.
  • Sustained arterial hypertension damages blood vessels in kidney, heart, and brain and leads to an increased incidence of renal failure, coronary disease, heart failure, stroke, and dementia.
  • The DIAGNOSIS of hypertension is based on repeated, reproducible measurements of elevated blood pressure.
  • Starting at 115/75 mm Hg, cardiovascular disease risk doubles with each increment of 20/10 mm Hg throughout the blood pressure range.


Systolic/Diastolic B.P.


< 120/80


< 139/89


> 140/90

Stage 1 Htn


Stage 2 Htn




  • A specific cause of hypertension can be established in only 10–15% of patients. Patients in whom no specific cause of hypertension can be found are said to have essential or primary hypertension (associated with high sodium/potassium and calcium intake ratio, genetic factors, psychological stress and environmental factors).
  • Patients with a specific etiology are said to have secondary hypertension (e.g. renal artery constriction, coarctation of the aorta, pheochromocytoma, Cushing’s disease, primary aldosteronism, etc) and are amenable to surgical correction.


  • Regulation of blood pressure in hypertensive patients differs from healthy patients in that the baroreceptors and the renal blood volume-pressure control systems appear to be “set” at a higher level of blood pressure. All antihypertensive drugs act by interfering with these normal mechanisms.

Postural baroreceptor mechanism

Renal regulation of blood pressure

Baroreflexes are responsible for rapid, moment-to-moment adjustments in blood pressure, such as in transition from a reclining to an upright posture.

Baroreceptor stretch activation inhibits central sympathetic discharge. Conversely, reduction in stretch results in a reduction in baroreceptor activity and regain of discharge.

The reflex increase in sympathetic outflow acts through nerve endings to increase peripheral vascular resistance (constriction of arterioles) and cardiac output (direct stimulation of the heart and constriction of capacitance vessels, which increases venous return to the heart), thereby restoring normal blood pressure.


By controlling blood volume, the kidney is primarily responsible for long-term blood pressure control.

A reduction in renal perfusion pressure causes intra-renal redistribution of blood flow and increased reabsorption of salt and water. In addition, decreased pressure in renal arterioles as well as sympathetic neural activity (via βeta- adrenoceptors) stimulates production of renin, which increases production of angiotensin II.

Angiotensin II causes (1) direct constriction of resistance vessels and (2) stimulation of aldosterone synthesis in the adrenal cortex, which increases renal sodium absorption and intravascular blood volume. Vasopressin released from the posterior pituitary gland also plays a role in maintenance of blood pressure through its ability to regulate water reabsorption by the kidney



  1. Diuretics: Thiazides: Hydrochlorothiazide, Chlorthalidone, Indapamide
    High ceiling: Furosemide,etc.
    K' Sparing: Spironolactone, Amiloride
  2. ACE inhibitors: Captopril, Enalapril, Lisinopril, Perindopril, Ramipril, Fosinopril,etc.
  3. Angiotensin (AT 1 receptor) blockers: Losartan, Candesartan, Irbesartan, Valsartan, Telmisartan
  4. Calcium channel blockers: Verapamil, Diltiazem, Nifedipine, Felodipine, Amlodipine, Nitrendipine, Lacidipine.
  5. Beta Adrenergic blockers: Propranolol, Metoprolol, Atenolol, etc.
  6. Alpha + Beta Adrenergic blockers: Labetalol, Carvedilol
  7. Apha Adrenergic blockers: Prazosin, Terazosin, Doxazosin, Phentolamine, Phenoxybenzamine
  8. Central sympatholytics: Clonidine, Methyldopa
  9. Vasodilators: Arteriolar: Hydralazine, Minoxidil, Diazoxide
    Arteriolar+ Venous: Sodium nitroprusside
  1. Ace Inhibitors
    2. Inhibit formation of Angiotensin-II
    3. Reduce Peripheral Vascular Resistance
    4. No effect on Cardiac Output 


  1. Well absorbed; captopril is best absorbed
  2. Moxipril, fosinopril---eliminated by bile (safe in renal disease)
  3. Enalapril, Lisinopril do not contain SH group
  4. Given till 3.5 mg/dl of creatinine clearance in renal failure
  5. Telandopril, ramipril---vessel selective drugs (stabilize plaque, anti-atherosclerotic activity)
  • HOPE (-Heart Outcome Prevention Evaluation-reduced mortality by 22%)



  1. HTN with CHF                
  2. CHF alone (Remodel myocardium)                        
  3. HTN in young
  4. Microalbuminuria
  5. DM with HTN                       
  6. Unilateral RAS
  7. Renovascular HTN      
  8. Hypertension in CRF                          
  9. Normal rennin hypertension



  1. MC-Dry Cough
  • Bradykinin mediated
  • Icatibant can be used (Bradykinin antagonist)
  • Losartan is an alternative
  1. Hyperkalemia (In renal dysfunction)
  2. Hypotension (not mediated by bradykinin); occurs due to inhibition of Ang-II formation
  3. Angioedema
  4. Proteinuria
  5. Agranulocytosis
  6. Dysgusia (Captopril)
  7. Rashes

Drug interaction

  1. NSAID’s blunt their antihypertensive actions
  2. Plasma levels of lithium get increased due to reduced tubular secretion.
  3. Plasma levels of digoxin get increased due to reduced clearance
  4. Given with diuretics, first dose hypotension is more
  5. Potassium sparing diuretics increase the risk of hyperkalemia


  1. Renal artery stenosis (B/L)          
  2. Pregnancy (FETOTOXIC)
  3. Renal failure                
  4. HOCM          
  5. Intestinal obstruction
  1. Angiotensin Receptor Blocker (ARB)
    1. Drugs:  Losartan, Omnesartan, Irbesartan, Velasartan
    2. Block AT1 receptor; Competitive blocker
    3. Same efficacy as ACE I but associated with more side effects, although two side effects are not seen i.e. cough and angioedema
    4. Eliminated by bile (liver) and partially from kidney
    5. Have Antiplatelet activity; stopped 24 hours before surgery
    6. Uricosuric-useful in gout with HTN
  2. Alpha-2 Agonists
    1. Clonidine                    
    2. Methyldopa        
    3. Gaunebenz            
    4. Gaunefacine
    5. Gaunethidine*        
    6. Guanedrel*
      1. *Last two are ganglion blockers
      2. Used in “pharmacological sympathectomy
  • In Colle’s fracture
  • Thyroid opthalmopathy where antithryoid drugs are not effective


  1. Clonidine, Methyl-Dopa (MC used)
  2. Reduce NE release from central neurons
    1. Bradycardia             
    2. Decrease CO
    3. PVR may increase in beginning due toalpha-2 stimulation of blood vessels
    4. Reduce rennin release


  1. Lipid soluble (Clonidine patches are available)
  2. Well absorbed
  3. High first metabolism
  • Methyl-Dopa forms a false neurotransmitter; Octapine, alpha methyl NE
  1. False NT hypothesis is not valid
  2. That means, False NTs are not responsible for decrease in BP


  • Clonidine
  1. Moderate to severe HTN
    1. HTN following opioid withdrawal
    2. Postmenopausal HTN
    3. Diabetic diarrhea
    4. Brimonidine is a prodrug of clonidine, used for gluacoma
    5. Recall; depivefrine is a prodrug of adrenaline, used for glaucoma
  • Alpha-Methyldopa: (Used in Hypertension in Pregnancy, Not used clinically now a days)
    Side effects of alpha-2 agonist:
  • Clonidine
  1. Dry mouth           
  2. Depression          
  3. Sedation
  4. Clonidine should not be stopped abruptly -rebound HTN -Rx-phentolamine
  • Prazosin can not antagonise the side effects as it is alpha-1 blocker; YOHIMBINE can antagonise (alpha-2 bloker)
  • Methydopa
  1. Autoimmune hemolytic anemia (Coomb’s test positive)
  2. Granulomatous hepatitis (All SHIP drugs, halothane, allopurinol)
  3. Hyperprolactinemia
  4. Extrapyramidal symptoms
  1. Sodium Nitroprusside
    1. Fastest, shortest acting                
    2. Half life=10-15 mins
    3. Venodilator, arterial dilator (Combined)
    4. MAO-same as nitrates (NO-cGMP)
    5. Given IV (0.5-10 mgm/kg)

Thiocyanate toxicity

  1. Prolonged infusion of nitropressuside causes Thiocyanate accumulation-cynosis (>10mg/dl)---seziures
  2. Hydroxoycobalamin can be used for Rx


  • DOC-HTN emergency


  1. Excessive hypotension
  2. Used for producing controlled hypotension
    1. Isoflurane is a substitute of this drug
    2. Halothane should be avoided, because hypotension is uncontrolled
  3. Arrhythmias
  1. Ganglion Blockers
  • Two types
  1. Simple (Competitive)
    1. Trimethophan      
    2. Hexamethonium  
    3. Mecylamine
  2. Complex (Non-competitive)
    1. Gaunedrel            
    2. Gaunethidine              
    3. Bretylium            
    4. Debrisoquin


Act competitively to block the ganglionic nicotinic receptors at postsynaptic junctions.

Simple blockers

  • Well absorbed (Mecylamine)
  • Others not absorbed-quaternary amines
    • Trimethophan is short acting (half life 1 hour), rapidly acting


  1. Mydriasis             
  2. Cycloplegia             
  3. Hypotension (Should be followed by tachycardia; Merry’s rule)
  4. Bradycardia        
  5. Diarrhea                
  6. Constipation              
  7. Impotence                  
  8. Fluid retention


  • Produces “pharmacological sympathectomy”
    • Hyperthyroid eye disease
    • Sudeck’s osteodystrophy (Occurs following Colle’s fracture)
  1. CCBs: Three types
    1. Dihydropyridines (DHP)
      1. Nifedipine            
      2. Amlodipine            
      3. Nicardipine        
      4. Nisoldipine
      5. Felodipine            
      6. Efonidipine          
      7. Nimodipine
    2. Phenylalkylamine
  • Verapamil
  1. Benzothiazines
  • Diltiazem  

*DHP are the most widely used CCB for hypertension, as they are least cardio-selective and have greatest effect on peripheral resistance



  1. Vasodilators
  2. Reduce PVR
  3. Block L type of calcium channels (Ca2+ channels are of 3 types: N, T, L)


  1. Well absorbed
  2. High first pass metabolism in liver
  3. Verapamil has flow dependent elimination
  4. Short acting drugs
    1. Nifedpine half life =1 hour
    2. Amlodipine half life=8 hours


  • CCBs (DOC)
  1. Low rennin HTN (High rennin HTN-beta-blockers, normal rennin-ACE I-MC type)
  2. Isolated systolic HTN
  3. Nifedipine-PVD
  4. Nimodipine-cerebroselctive-SAH
  5. Efonidipine-new drug for atrial arrhythmias
  6. Nicardipine- cardio selective CCB


  1. MC s/e Ankle edema-diuretic responsive
  2. GERD
  3. Constipation
  4. Hypotension
  5. Bradycardia (Verapamil, diltizem-node selective drugs)
  6. Reflex tachycardia with nifedipine-not used in HTN emergency
  7. GLUE neutral drugs (means, do not affect levels of these chemicals)
    1. Glucose        
    2. Lipid            
    3. Uric acid              
    4. ​Electrolytes
  1. Arteriolar Dilators
    1. Dizoxide              
    2. Minoxidil              
    3. ​Hydralazine


Pure arteriolar dilators

  1. Minoxidil- K+ opener                            
  2. Diazoxide- K+ opener    
  3. Hydralazine- MAO is same as nitrates


  1. Short acting          
  2. Rapid first pass metabolism
  3. Half lives=1 hour        
  4. Minoxidil is eliminated by bile


  1. Hypertensive emergencies
  2. Minoxidil-male pattern baldness; finasteride is also used
  3. Diazoxide is used in the treatment of Insulinoma


  1. Hypotension is MC              
  2. Reflex tachycardia-C/I IHD                  
  3. Dizoxide-hyperglycemia
  4. Minoxidil - hypertrichosis              
  5. Fluid retention                              
  6. Hydralazine-SLE
  7. Increase rennin

Mechanism Of Action Of Vasodilators:



Release of nitric oxide from drug or endothelium


Nitroprusside, Hydralazine, Nitrates, Histamine, Acetylcholine

Reduction of calcium influx

Verapamil, Diltiazem, Nifedipine

Hyperpolarization of smooth muscle membrane through opening of potassium channels

Minoxidil, Diazoxide

Activation of dopamine receptors



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