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ANTI HYPERTENSIVE DRUGS

This document discusses various types of antihypertensive drugs including diuretics, renin-angiotensin system inhibitors, sympathetic inhibitors, calcium channel blockers, and vasodilators. It describes the mechanisms of action, pharmacological effects, drug interactions, and side effects of common antihypertensive drugs from each class such as hydrochlorothiazide, captopril, propranolol, nifedipine, and hydralazine. The document provides an overview of classifications, treatment approaches, and management of hypertension using different antihypertensive drug classes and combinations.

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ANTI HYPERTENSIVE presented by-Subham Mishra
INTRODUCTION:  Hypertension-Elevation of systolic and diastolic blood pressure.  It is also known as silent killer.  Normal BP-120/90 mm/hg Types of Hypertension : 1.Primary Hypertension-causes are unknown 2.Secondary Hypertension-causes are known Examples-kidney prblms Aldosteronism Thyroid prblms coarchtation of aorta by birth.
Risk factors: 1.Age-Risk increase with age 2.Family history. 3.Obesity 4.Smoking 5.Stress conditions. Classifications: 1.Diuretics: a. Thiazide diuretics- Hydrochlorthiazide, Indapamaide, chlorthalidone. b. Loop diuretics- Furosemide c. Aldosterone antagonist-Spironolactone, Eplerenone 2. Renin-Angiotensin system inhibitors: a. Ace inhibitors: Captopril, Enalapril, Lisnopril, Ramipril b.AT1 blockers- Losartan, candesartan, Temisartan, Olmesartan c. Direct Renin Inhibitors- Aliskiren
3.Sympathetic inhibitors: a. A-Blocker- Prazocin, Terazocin b. B-blocker- Propranolol, Metaprolol, Atenolol c. Mixed sympatholytics-Labetalol,Carvedilol d. Central sympatholytics-clonidine,methyldopa,Guanefine 4.Calcium channel blockers:-Verapamil,Diltiazem,Nifedipine 5.Vasodilators- Hydrolazine, Minoxidil, Nitroprusside sodium
DIURETICS:  Hydrochlorthiazide and chlorthalidone are the DOC of complicated hypertension.  Chlorthalidone is longer acting(48hrs),and HCZ is 24 hrs and may be have better round clock action.  Indapamide is also mainly used as antihypertensive and is equally effective.  FUROSEMIDE is a strong diuretic but a weaker hypertensive drug than thiazide the natriuretic action lasting only for 4-6 hrs after the conventional morning dose is followed by compensatory mechanism in proximal tubular reabsorption of sodium. MECHANISM OF ACTION: o Thiazide diuretics decreases sodium-water retention leads to decrease in blood volume then the cardiac output decreases. o With long term treatment the plasma volume approaches normally but total peripheral resistance decreases. o Potassium sparing diuretics and thiazide diuretics leads to decrerase in amount of potassium loss.
PHARMACOKINETICS PROFILE: -Fall in B.P develops after 2-4 weeks. -They are more effective elderly. -Max antihypertensive activity is 25mg/day. -Indapamide is well absorbed orally has an elimination of 16 hr. -Thiazide diuretics can be combined with B-blocker+ACE+AT1 blocker  ADVERSE EFFECTS: 1.Hypokalemia-muscle pain,fatigue 2.Erectile dysfunction. 3.Carbohydrate intolerance. 4.Dyslipidemia 5.Hyperuricemia 6.Acute Gout attack-due to compete with uric acid for elimination.
RENIN-ANGIOTENSIN SYSTEM INHIBITORS. MECHANISM OF ACTION: -LIVER secrete ANGIOTENSINOGEN and it is converted to Angiotensinogen-1 by RENIN which is secreted by kidney. -ANGIOTENSINOGEN-I is converted to ANGIOTENSINOGEN-II by ACE which is secreted by LUNGS. -ANGIOTENSINOGEN binds to its specific receptor then it forms ALDOSTERON by ADRENAL CORTEX then again action occurs and B.P increases.. -TO decrease blood volume or peripheral resistance or cardiac output. We have to give Renin inhibitors-ALISKIREN therefore no Angiotensinogen-I formed. We can give ACE inhibitors to inhibtion of secretion of ACE. Therefore no secretion of ANG-II.LEADS to vasoconstrictor. We can give AT1 blocker to stop the binding of anginotensinogen to the receptor. In this way we can give Renin angiotensin system inhibitors to decrease peripheral resistance and vascular cardiac output. -It also decreases Breakdown of Bradykinin leads to increase of Nitric oxide and prostacycline leads to Potent VASODILATOR.
PROTOTYPE DRUGS:CAPTOPRIL -It is a dipeptide,sulphyhydral containing proline surrogate, ACE. MECHANISM OF ACTION: -Inhibition of vasoen endothelial kinmase-II enzyme and prevents the conversion of ANG-I TO ANG-II. PHARMACOKINETIC PROFILES: Well absorbed orally , converted into active forms in liver and excreted through kidney. INTERACTIONS; -NSAID inhibits Hypotensive action. -Hypokalaemia -Antacids reduce bioavailability. -Lithium clearance inhibited. CONTRAINDICATION: Pregnancy due to teratogenic effect. Dose: 25-50 mg/BD/TDS/1hr before or 2hr after a meal.
ADVERSE EFFECTS: -Acidosis -Hyperkalemia -Stomatitis -Tachycardia -Angioedema -Vertigo. USES: -Hypertension -Myocardial infraction. -Diabetic neuropathy -Progressive renal insufficiency.
SYMPATHETIC INHIBITOR: Beta blocker : MECHANISM OF ACTION: -Beta blocker decrease blood pressure by decreasing cardiac output. -It also decreses sympathetic outflow in CNS. -It also decreases release of Renin from kidney , therefore ANG-II decreses secretion of Aldosteron. -prototype Beta blocker-PROPRANOLOL,Act on Beta 1 and 2 receptor. -Selective Beta -1 blocker are Metaprolol and Atenolol. -Nebivolol increase production of nitric oxide leads to dilation. -Selective Beta blocker must be used cautiously in case of asthma patients. -Non selective Beta blocker propranolol are not be used in Asthmatic patients due to their blockade of Beta2 mediated leads to vasodilTION.
ALPHA-2 BLOCKER:CLONIDINE -It is centrally acting Alpha-2 adrenergic agonist agent,useful in the treatment of essential hypertension. PHARMACOLOGICAL ACTION: -Enhanced parasympathetic activity and vagal tone. -Increases growth hormone level but decreases insulin secretion. -It produces sedation. -It causes Hypothermia. MECHANISM OF ACTION: -It decreases heart rate, cardiac output, peripheral resistance and peripheral resistance and plasma renin activity by inhibiting release of adrenaline from the nerve endings or suppressing sympathetic tone, due to stimulation of al[pha-2 adrenergic receptors in the brain. PHARMACOKINETICS PROFILE: -Well absorbed from GIT after oral administration , almost half metabolized in liver and remaining excreted as such in urine.
DOSE-2-4mg/day/orally. ADVERSE EFFECTS: -Anxiety -Bradycardia -Depression -Gynaecomastia -Nightmares -Myalgia -Nasal stiffness. -Raynauds phenomenon USES: -Essential hypertension -Migraine -Diagnosis of pheochromocytoma
CALCIUM CHANNEL BLOCKER: CLASSIFICATION:  Phenylalkamine - Verapramil  Benzothiazepine- Diltiazem  Dihydropyridine- Nifedipine, Amlodipine, Felodipine MECHANISM OF ACTION:  Voltage sensitive channel activated when potential drop to -40mv.  Receptor operated due to activation of Adrenaline and other agonist.  Small amount of calcium leak into resting cell and pumped out by calcium ATPase and mechanical stretch allows it.  There are 3 types of voltage sensitive calcium channels- 1-L-type-long acting current 2-T-type-Transient current 3.N-type-Neuronal current.
-Action of calcium blocker in Arterioles only : 1.Smooth muscle relaxation. 2.Decrease heart rate.  Inhibition of calcium ion influx. PHARMACOLOGICAL ACTION:  Reduces oxygen demand by suppressing contractility and rate of heart.  Dilate coronaries and peripheral arteries. ADVERSE EFFECTS- 1-Depression 2.Parkinsonism 3.Gynaecomastia 4.Bradycardia 5.Sino-atrial block 6-palpitation. USES; 1.Angina 2.Atrial fibrillation 3.PSVT 4.MI
VASODILATORS: MECHANISM OF ACTION;  Produce relaxation of vascular smooth muscles.  This relaxation decreses the peripheral resistance leads to decrease in blood pressure.  Activation of potassium channels leads to increase in potassium efflux.  Increase in Efflux leads to Hyperpolaraisation of smooth muscle.  Membrane hyperpolarised leads to decrease in calcium influx.  Decrease in calcium influx leads to Arteriolar dilation.  Then it produce reflux stimulation of Heart. ADVERSE EFFECTS:  Produce reflux stimulation of heart.  Result in competing reflux of myocardial contraction, Heart rate and oxygen contraction.  It may cause Angina, MI.
INTERACTIONS:  MAO inhibitors , Tricyclic Antidepressants, Diuretics. CONTRAINDICATION:  Severe Tachycardia  Heart failure. DOSE: 100-200 mg/TDS/orally. USES:  Agitation.  Arthalgia  Tachucardia  Tachyphylaxis  Nasal stiffness.
THANK YOU REFERENCES:  Essential of medical pharmacology 8th edition-KD TRIPATHY.  Lipincott pharmacology.  Drugs pharmacology by Kamal Kishore maheswari.