Hypertension

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By: vsdesai (20 month(s) ago)

Pl send your prsntn on vsdesai@rediffmail.com & oblige. Dr Desai , Mumbai

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Hypertension: The Silent Killer:

Hypertension: The Silent Killer Hypertension- asymptomatic & multifactorial Morbidity and mortality due to end organ damage Hypertension leads to Heart Attack Stroke Kidney Failure

Types of Hypertension:

Types of Hypertension Primary hypertension (90-95%) (Essential Hypertension – Patients in whom no specific cause of hypertension can be found are said to have essential hypertension ) Secondary Hypertension (5-10%)

Etiology of Primary Hypertension:

Etiology of Primary Hypertension Genetics (African American background) Hyperlipidemia Family history Dietary factors (increased salt intake) Diabetes Obesity Aging Psychological stress (worry, tension) Excessive alcohol intake & smoking

Etiology of Secondary Hypertension:

Etiology of Secondary Hypertension 1. Renal diseases 2. Endocrine Diseases Steroid excess - Hyperaldosteroism (Conn’s syndrome) - Hyperglucocorticodism (Cushing’s Syndrome) Catecholamine excess - Pheochromocytoma Growth hormone excess - Acromegaly

Treatment Strategy for Hypertension:

Treatment Strategy for Hypertension 1. Diagnosis 2. Determination of primary vs. secondary hypertension 3. If secondary, treat underlying pathology 4. If primary, initiate lifestyle changes smoking cessation weight loss / diet control stress reduction less alcohol 4. Pharmacological treatment

PowerPoint Presentation:

Blood Pressure = Cardiac Output X Peripheral Resistance Preload Contractility Heart Rate Circulating Fluid Volume Renal Sodium Handling Sympathetic Nervous System Renin Angiotensin Aldosterone System Arteriolar Venous Vasoconstriction Venous Vascular Smooth Muscle Vascular remodeling Determinants of Arterial Pressure

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Determinants of Arterial Pressure Mean Arterial Pressure = X Arteriolar Diameter Blood Volume Stroke Volume Heart Rate Filling Pressure Contractility Blood Volume Venous Tone CRITICAL POINT! Change any physical factors controlling CO and/or TPR and MAP can be altered.

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V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules Total Peripheral Vascular Resistance (TPVR) Ang I Cardiac Output Heart a 2 TPVR VSMCs Vascular Smooth Muscle Cells

Antihypertensive Agents:

Antihypertensive Agents Diuretics Calcium Channel Blockers Angiotensin Converting Enzyme Inhibitors Angiotensin Receptor Antagonists Peripheral Vasodilators Sympatholytic Drugs Alpha-1 Blockers Beta Blockers Alpha-2 Agonists Ganglionic Inhibitors Adrenergic Neural Terminal Inhibitors

Diuretics:

Diuretics

Diuretics:

Diuretics Thiazides and thiazides-like diuretics Aldosterone antagonists Potassium sparing diuretics Loop diuretics ++++ ++ + +

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Inhibition of Sodium Reabsorption Reduced Circulating Volume Reduced Preload Reduced Cardiac Output Diuretics

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V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 DIURETICS VSMCs

Diuretics: Thiazides :

Diuretics: Thiazides Initial effects: diuresis, (reduced extracellular and circulating volume) Chronic effect: reduction in peripheral vascular resistance (direct vasodilating effect) African Americans, elderly, obese Combination with ACEIs and beta blockers Given once daily

Diuretics: Thiazides :

Diuretics: Thiazides Distal Convoluted Tubule - Na/Cl Symport Inhibitors Bendroflumethiazide [NATURETIN] Benzthiazide [EXNA] Chlorothiazide [DIURIL] Hydrochlorothiazide [HYDRODIURIL] Hydroflumethiazide [SALURON] Methyclothiazide [ENDURON] Polythiazide [RENESE]

Diuretics: Thiazides-like :

Diuretics: Thiazides-like Distal Convoluted Tubule - Na / Cl Symport Inhibitors Sulfonamide related compounds Chlorthalidone [HYGROTON] Indapamide [LOXOL] Metolazone [MYKROX, ZAROXOLYN] Longer acting and more powerful .

Diuretics: Thiazides:

Diuretics: Thiazides Side Effects At low doses thiazides are well tolerated Hypokalemia Lipid elevation Glucose intolerance Hyperuricemia Hypercalcemia Very rarely: severe rash, tombocitopenia and leucopenia.

Diuretics: Thiazides :

Diuretics: Thiazides YES: (useful in) Elderly patients African Americans Patient with mild or incipient heart failure When cost is crucial When salt intake is high Sexually active females Combined with other first line antihypertensive drugs No: (avoid in) Patients with NIDDM Patients with hyperlipidemia Patients with gout Sexually active males Glomerular Filtration Rate < 30ml/min

PowerPoint Presentation:

Potassium-Sparing Diuretics Amiloride [MIDAMOR]; Triamterene [DYRENIUM, MAXZIDE] Second line anti-hypertensive drugs Used in combination, or for correction of hypokalemia Diuretics Loop of Henle Fuosemide [LASIX]; Bumetanide [BUMEX]; Ethacrynic Acid [EDECRIN]; Torsemide [DEMADEX] Second line anti-hypertensive drugs Used in hypertensive patient with chronic renal disease for volume/salt control

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Aldosterone Antagonists

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V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Aldosterone Antagonists VSMCs

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Aldosterone Antagonists Aldosterone Functions: Classical Renal-Ion Transport Site of Action: Collecting duct Increases Na ++ reabsorption (Active) Increases K + excretion (Passive?) Increases H + excretion (Active & passive)

Spironolactone [ALDACTON®] - Hyperaldosteronism - In severe heart failure (NYHA Class IV), improves survival and reduces hospitalization (RALES Study) - Hyperkalemia, Gynecomastia Eplerenone [ INSPRA® ] - Hypertension and post-MI heart failure (EPHESUS study) - Anti-oxidant effects (?) - Less adverse effects (gynecomastia) - More expensive :

Spironolactone [ ALDACTON ® ] - Hyperaldosteronism - In severe heart failure (NYHA Class IV), improves survival and reduces hospitalization (RALES Study) - Hyperkalemia, Gynecomastia Eplerenone [ INSPRA ® ] - Hypertension and post-MI heart failure (EPHESUS study) - Anti-oxidant effects (?) - Less adverse effects (gynecomastia) - More expensive Aldosterone Antagonists

Beta Blockers ( … lol):

Beta Blockers ( … lol)

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V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 b - Blockers VSMCs ? ?

Beta Blockers Mechanisms and Sites of Action:

Beta Blockers Mechanisms and Sites of Action Negative Chronotropic & Inotropic Effects Inhibition of Renin Release ______________________________ - Reduction in cardiac output - Inhibition of renin release - CNS effects - Reduction in venous return and plasma volume - Reduction in peripheral resistance - Improvement in vascular compliance - Resetting of baroreceptor levels - Effects on prejunctional b 2 receptors - Attenuation of pressor response to catecholamines (stress, exercise) ______________________________

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Cardioselectivity (Beta-1 vs Beta-2 ) Intrinsic Sympathomimetic Activity (ISA; partial agonistic activity) Affinity for alpha-1 adrenergic receptors (Labetalol, Carvedilol) Beta Blockers

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There are 15 Beta blockers in the market Approved for hypertension (13) and for one or more of following indications: Angina pectoris Myocardial Infarction Ventricular arrhythmia Migraine prophylaxis Heart Failure Perioperative Hypertension Beta Blockers

Beta Blockers ( …lol):

Beta Blockers ( …lol) Beta-1,2-Non-Selective Propranolol [INDERAL] Nadolol [CORGARD] Carteolol [CARTROL] * Timolol [BLOCADREN] Pindolol [VISKEN] * Sotalol [BETAPACE] Penbutol [LEVATOL] * Beta-1-Selective Acebutolol [SECTRAL] * Atenolol [TENORMIN] Betaxolol [KERIONE] Bisoprolol [ZEBETA] Esmolol [BREVIBLOC] Metoprolol [LOPRESSOR ] Beta-1,2/Alpha 1Selective Labetalol [TRANDATE, NORMODYNE] Carvedilol [COREG] * - ISA X X

PowerPoint Presentation:

Side Effects: Bronchospasm Bradicardia/heart block Mask and prolong the symptoms of hypoglycemia Abrupt withdrawal can precipitate MI Cold extremities, Raynaud’s phenomenon, intermittent claudication Decreased exercise tolerance; fatigue, depression and impotence CNS: sleep disturbance, vivid dreams, nightmares Effects of plasma lipids Beta Blockers

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YES: (useful in) Younger patients Anxious patients Angina pectoris Post-MI patient Beta Blockers No: (avoid in) Patients with COPD IDDM Pateints with peripheral vascular disease Raynaud’s syndrome 2nd and 3rd degree block Energetic patients

Angiotensin Converting Enzyme Inhibitors (ACEIs):

Angiotensin Converting Enzyme Inhibitors (ACEIs)

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 ACE I nhibitors VSMCs

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Angiotensinogen Ang I Ang II Renin (renal) Renin Angiotensinogen Angiotensinogen Ang I mRNA A T 1 Ang II A T 1 A C E ACE ( autocrine) ( paracrine) (endocrine) mRNA Renin mRNA A C E endothelial cell tissue (VSM cells) (myocyte ) (liver) mRNA A C E mRNA mRNA Renin Angiotensinogen Angiotensinogen Ang I ACE Ang II Local (tissue) RAS: Intrinsic; Extrinsic blood vessel

ACE Inhibitors Antihypertensive Mechanisms :

ACE Inhibitors Antihypertensive Mechanisms Inhibition of circulating RAS Inhibition of tissue and vascular RAS Modulation of sympathetic activity Decreased formation of endothelin from endothelium Increased formation of bradykinin and vasodilatory prostaglandins Decreased sodium retention (decreased aldosterone secretion, and/or increased renal blood flow)

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Bradykinin A C E Kallikrein Renin Angiotensin II Angiotensin I Angiotensinogen Angiotensin Converting Enzyme ACEIs Kininogens Inactive Peptides BK receptors AT-1 receptors ACEIs

ACE Inhibitors ( … pril):

ACE Inhibitors ( … pril) Captopril [CAPOTEN] Enalapril [VASOTEC] Lisinopril [PRINIVIL, ZESTRIL] Benazepril [LOTENSIN] Fosinopril [MONOPRIL] Quinapril [ACCUPRIL] Ramipril [ALTACE] Spirapril [RENOMAX] Moexipril [UNIVASC] Perindopril [ACEON] Trandolapril [MAVIK]

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ACE Inhibitors Indications 80’s - Hypertension 90’s - Heart Failure ‘95 - Left Ventricular Dysfunction ‘95 - Diabetic Nephropathy ‘96 - Acute Myocardial Infarction

ACE Inhibitors: ( … pril):

ACE Inhibitors: ( … pril) Side effects Cough Hypotension Hyperkalemia Angioedema Renal Insufficiency Fetal injury (2 nd & 3 rd trimesters) “High-dose Captopril” Adverse effects ( Neutropenia, Impaired taste, Proteinuria )

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YES: (useful in) Younger patients Post MI LV dysfunction Patient with heart failure Diabetic patients Non-diabetic nephropathy Metabolic disorders (hyperlipidemia, gout) ACE Inhibitors ( … pril) No: (avoid in) Renal artery stenosis Fluid-depleted patients Pregnancy Premenopausal women who may become pregnant

Angiotensin Receptor Blockers (ARBs):

Angiotensin Receptor Blockers (ARBs)

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 b 2 a 1 b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Ang II Receptor Blockers VSMCs Ang II Ang II

PowerPoint Presentation:

Sartans are selective and competitive antagonists of angiotensin II type 1 (AT 1 ) receptors and do not inhibit AT 2 receptors The physiological function of angiotensin II is mediated by AT 1 receptors (vasoconstriction, catecholamine release, aldosterone synthesis, and renal sodium and water retention) Blockade of AT 1 receptors increases plasma levels of Angiotensin I, Angiotensin II, and PRA Ang II Receptor Blockers (...sartans)

PowerPoint Presentation:

Actions of Angiotensin II Site of Action Cellular Effect Consequence Myocyte, IP 3 and Ca ++ increase Constriction Cardiocyte Protein kinase C Expression of proto- Fibroblast stimulation oncogenes; cell growth Sympathetic Nerve Endings Enhanced NE release Enhanced Vasoconstriction Glomeruli Efferent arteriolar Promotes constriction microalbuminuria Enlarges glomerular pores Proteinuria Juxtaglomerular Renin inhibition Relief of raised Apparatus intraglomerular pressure Adrenal Cortex Synthesis of Aldosterone Increased sodium retention and kaliuresis Fibrinolytic Increase of plasminogen Impaired fibrinolysis System activator inhibitor-1

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A n g i o t e n s i n II Peripheral resistance Renal function Cardiovascular structure Rapid Pressor Response 1. Direct vasoconstriction 2. Enhancement of peripheral noradrenergic neurotransmission 3. Increased central (CNS) sympathetic discharge 4. Release of catecholamines from adrenal medulla 1. Increases Na + reabsorption 2. Releases aldosterone from adrenal cortex 3. Altered renal hemodynamics : - renal vasoconstriction - increased noradrenergic neurotransmission in kidney - Increased renal sympathetic tone (CNS) Slow Pressor Response Cardiovascular Hypertrophy and Remodeling 1. Non-hemodynamic effects: - Increased expression of proto-oncogenes - Increased production of growth factors - Increased synthesis of extracellular matrix proteins 2. Hemodynamic effects: - Increased afterload (cardiac) - Increased wall tension (vascular)

Ang II Receptor Blockers (...sartans):

Ang II Receptor Blockers (...sartans) Losartan [COZAAR] Valsartan [DIOVAN] Irbesartan [AVAPRO] Candesartan [ATACAND] Eprosartan [TEVETEN] Tasosartan [VERDIA] Telmisartan [MICARDIS]

Ang II Receptor Blockers (...sartans):

Ang II Receptor Blockers (...sartans) Side effects Dizziness Angioedema has been reported rarely Hyperkalemia, comparable with that seen in patients treated with ACEIs Risk of fetal injury and death; should not be use during the 2nd and 3rd trimester of pregnancy Risk of symptomatic hypotension in hypovolemic patients Except for the absence of cough, Yes (useful in) and No (avoid in) same as for ACE inhibitors

ACE and Non-ACE Pathways of Angiotensin II Production:

ACE and Non-ACE Pathways of Angiotensin II Production Non-Renin Pathway Cathepsin G and Tonin Angiotensinogen Ang I Ang II Renin ACE Non-Renin Pathway Chymase

Calcium Channel Blockers (CCBs:

Calcium Channel Blockers (CCBs

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Calcium Channel Blockers Ca ++ L-type Ca ++ channels AV b 1

Calcium Channel Blockers Mechanisms and Sites of Action:

Calcium Channel Blockers Mechanisms and Sites of Action Negative Inotropic and Chronotropic Effects Produce Vasorelaxation at Arterioles Reduced Peripheral Resistance Verap+Dilti>Nifed Nifed>Dilti+Verap Block transmembrane entry of calcium into arteriolar smooth muscle cells and cardiac myocytes thus inhibiting excitation-contraction L-type Ca ++ channels

Calcium Channel Blockers:

Calcium Channel Blockers Dihydropyridines * Amlodipine [NORVASC] Felodipine [PLENDIL] Isradipine [DYNACIRC] Nicardipine [CARDENE] Nimodipine [NIMOTOP] Nifedipine [PROCARDIA, ADALAT] * Phenylalkylamine Verapamil [CALAN, ISOPTIN,VERELEN] Benzothiazepine Diltiazem [CARDIZEM, DILACOR] * long-acting or slow-release formulations should be used for high blood pressure

PowerPoint Presentation:

Pharmacologic Effects of Calcium Channel Blockers Effect Verapamil Diltiazem Dihydropyridines Peripheral Vasodilation ↑ ↑ ↑↑ Heart Rate ↓↓ ↓ ↑ Cardiac Contractility ↓↓ ↓ 0 / ↓ SA / AV Nodal Conduction ↓ ↓ 0 Coronary Blood Flow ↑ ↑ ↑↑ Calcium Channel Blockers

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Side effects Facial Flushing Headaches Non-pitting ankle edema Constipation Increased CHD mortality controversy: 1995 vs. 1997-2000 data (SYST-EUR study) Calcium Channel Blockers

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YES: (useful in) Elderly patients African Americans Patients with peripheral vascular disease Patients with cerebrovascular disease Patients with angina pectoris No: (avoid in) Patients with heart failure Patients with heart block Patients receiving b -blockers Short-acting dihydropiridines: Unstable angina Recent MI Calcium Channel Blockers

a1 - Adrenergic Receptors Blockers :

a 1 - Adrenergic Receptors Blockers

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 a 1 Receptors Blockers b 1 a 1 a 1 a 1 a 1

a1- Receptor Blockers:

a 1 - Receptor Blockers Inhibition of Vasoconstriction Induced by Endogenous Catecholamines at Arterioles and Veins Reduced Peripheral Resistance and Reduced Preload

PowerPoint Presentation:

Prazosin [MINIPRESS] Terazosin [HYTRIN] Doxazosin [CARDURA] [ Tamsulosin [FLOMAX] for BPH] Old drugs Alpha-1 + Alpha 2 Blockers Phenoxybenzamine [DIBENZYLIN] Phentolamine [REGITINE ] a 1 - Receptor Blockers

PowerPoint Presentation:

Side effects: First dose hypotension Dizziness, lethargy, fatigue Palpitation, syncope Peripheral edema Incontinence ALLHAT study results: Not to be used as first-line agents a 1 - Receptor Blockers

Central a2–Agonists:

Central a 2 –Agonists

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Central a 2 Agonists b 1 VSMC X X X X X

PowerPoint Presentation:

Diminished CNS Sympathetic Outflow Alpha-2 Agonist NE & EPI Pre-synaptic Neuron Alpha-2 Receptor Alpha-1 Receptor Beta Receptor Post-synaptic Effector Activation of Pre-synaptic Alpha-2 Receptors Reduces NE & EPI Release at Synapse Rostral Ventrolateral Medulla Central a 2 –Agonists

PowerPoint Presentation:

Clonidine [CATAPRES] Methyldopa [ALDOMET] Old drugs: [ Guanfacine [TENEX] ] [ Guanabenz [WYTENSIN] ] Central a 2 –Agonists

Peripheral Vasodilators:

Peripheral Vasodilators

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Peripheral Vasodilators b 1 NO → cGMP → Ca ++ b 2 a 1

PowerPoint Presentation:

Peripheral Vasodilators Ca 2+ - channel blockers Dihydropiridines Verapamil Diltiazem Ca2+ NO Activators of NO/guanylate cyclase pathway Hydralazine ? Nitroprusside Nitroglycerin K + - channels activators Minoxidile Diazoxide a 1 – Adrenoreceptor antagonists Doxazosin Prazosin K + Ang II receptor antagonists Losartan VSMCs

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Hydralazine [APRESOLINE] Minoxidil [LONITEN] *** Sodium Nitroprusside Diazoxide Peripheral Vasodilators

PowerPoint Presentation:

Hydralazine Arteriolar vasodilation by mechanism not well-defined (NO ?) Minoxidil Arteriolar vasodilation by activation of ATP-modulated potassium channels resulting in hyperpolarization of arteriolar VSMCs Second-third line of drugs for hypertension Induce reflex tachycardia, fluid and sodium retention Have be combined with first-line antihypertensive drugs Peripheral Vasodilators

PowerPoint Presentation:

Hydralazine: In slow acetilators, “lupus-like” syndrome (arthralgia, myalgia, skin rashes, and fever). For patients with CHF, pre-eclampsia Minoxidil: ”Last choice” for treatment of hypertension Minoxidil: Headache, sweating, and hirsutism, Topical minoxidil (Rogaine) used for correction of baldness. Peripheral Vasodilators

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V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Autonomic Ganglionic Inhibitors b 1 VSMC X X X X

Autonomic Ganglionic Inhibitors:

Autonomic Ganglionic Inhibitors Mecamylamine [INVERSINE]

Autonomic Ganglionic Inhibitors Mechanisms and Sites of Action:

Autonomic Ganglionic Inhibitors Mechanisms and Sites of Action Autonomic Ganglionic Inhibitor Acetylcholine Pre-ganglionic Neuron Ganglionic ACh Receptor Post-ganglionic Neuron Inhibit neurotransmission in autonomic ganglia by competing with acetylcholine for ganglionic cholinergic receptor sites. Reduced peripheral resistance and venous return

PowerPoint Presentation:

V V Vasomotor center Afterload Volume Kidneys Preload Renin Ang II Aldosterone BP= CO x TPVR b 1 Resistance arterioles Capacitance venules TPVR Ang I Cardiac Output Heart a 2 Adrenergic Neural Terminal Inhibitors b 1

Adrenergic Neural Terminal Inhibitors:

Adrenergic Neural Terminal Inhibitors Reserpine Guanethidine [ISMELIN] Guanadrel [HYCOREL] Metyrosine [DEMSER]

PowerPoint Presentation:

Reserpine: binds to catecholamine storage vesicles in peripheral and central neurons, rendering them unable to store or release NE and EPI Guanethidine and Guanadrel: stored in peripheral neurosecretory granules and released as “inactive” neurotransmitter in place of NE and EPI Metyrosine: reduces catecholamine biosynthesis in peripheral nerves and adrenal by inhibiting rate-limiting enzyme, tyrosine hydroxylase Adrenergic Neural Terminal Inhibitors

Combination Drugs in Hypertension :

Combination Drugs in Hypertension ACE Inhibitor + Diuretic Benazepril + HCTZ ( Lotensin HCT ® ) Captopril + HCTZ ( Capozide®) Enalapril + HCTZ (Vaseretic ® ) Lisinopril + HCTZ ( Prinzide ®, Zestoretic ® ) Moexipril + HCTZ ( Uniretic ® ) Quinapril + HCTZ ( Accuretic ® ) Ang II Receptor Antagonist + Diuretic Losartan + HCTZ( Hyzaar ® ) Irbesartan +HCTZ( Avalide ® ) Valsartan + HCTZ ( Diovan HCT™ )

Combination Drugs in Hypertension :

Combination Drugs in Hypertension Beta-Blocker + Diuretic Atenolol + Chlorthalidone ( Tenoretic ®) Bisoprolol + HCTZ ( Ziac™ ) Metoprolol + HCTZ ( Lopressor ® HCT ) Propranolol + HCTZ ( Inderide ®, Inderide ® LA ) Timolol + HCTZ (Timolide ® ) Betaxolol + Chlorthalidone ( Kerledex ® ) Labetalol + HCTZ ( Normozide ®, Trandate ® HCT )

Combination Drugs in Hypertension :

Combination Drugs in Hypertension ACE Inhibitor + Calcium Channel Blocker Amlodipine + Benazepril (Lotrel ® ) Enalapril + Diltiazem ( Teczem ® ) Felodipine + Enalapril ( Lexxel ® )

Combination Drugs in Hypertension :

Combination Drugs in Hypertension Alpha-1 Blocker + Diuretic Prazosin + Polythiazide ( Minizine ® ) Alpha-2 Agonist + Diuretic Clonidine + Chlorothalidone ( Combipress ® ) Methyl-dopa + HCTZ ( Aldoril ® ) Neuronal Terminal Inhibitor + Diuretic Reserpine + HCTZ ( Hydropress ® ) Reserpine + Chlorthalidone; Reserpine Demi- Regroton®, Regroton® Guatethidine + HCTZ ( Esimil ® )

PowerPoint Presentation:

Diuretics Beta Blockers ACE Inhibitors Calcium Channel Blockers AT 1 Receptor Antagonists Alpha 1 Blockers Alpha 2 Agonists Vasodilators Oral Antihypertensive Agents: Summary