Drug Treatment of Hypertension
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1 Drug Treatment of Hypertension Medical Pharmacology Lectures 41 & 42 Marcelo G. Bonini Department of Pharmacology College of Medicine Tel / Room 3035 COMRB
2 Definition: or Systolic BP 140 mm Hg Diastolic BP 90 mm Hg Diagnosis is based on multiple ( 3) measurements, on different days For patients having diabetes or chronic kidney disease (high-risk group), diagnosis of hypertension is made with BP 130/80 mmhg
3 Classification and management of BP for adults Category Systolic Diastolic Lifestyle modification Initial drug therapy Normal < 120 and < 80 Encourage Not needed Pre-hypertension or Yes No, or treat Compelling indications Stage 1 hypertension or Yes Diuretic, ACEI, ARB, β-blocker, CCB, Combination; + compelling indications Stage 2 hypertension 160 or 100 Yes Two-drug combo (diuretic and ACEI, or ARB or β-blocker or CCB; Also treat compelling indications Based on 7 th Report of the Joint National Committee on Detection, Evaluation, and Treatment of High BP (JNC 7) Diuretic here means thiazide-type; ACEI, ACE inhibitor; ARB, angiotensin receptor blocker; β-blocker, β-adrenergic receptor blocker; CCB, calcium channel blocker
4 Present vs optimal systolic BP distribution Increased longevity, physical inactivity, obesity and unhealthy diet contribute to the right-shift of the curve. Data from WHO, 2003
5 Hypertension is a leading global risk factor for mortality Hypertension affects 65 millions in the U.S. (NIH estimation) The Lancet, 360:1347 (2002)
6 BP = CO PVR CNS / sympathetic nerves Baroreceptor reflex arc Aortic arch carotid sinuses Heart rate contractility β1-ar Peripheral resistance α1-ar Arterial Blood Pressure Cardiac output Na + /Ca 2+ exchange Baroreceptors Stroke volume Reninangiotensinaldosterone Sodium/ volume Venules capacitance
7 BP = CO PVR and MAP = CO TPR MAP = Mean Arterial Pressure = (SBP DBP) / 3 + DBP CO = Cardiac Output TPR = Total Peripheral Resistance
8 Factors affecting drug treatment of hypertension: Accuracy of diagnosis; severity of hypertension Etiology: Primary (essential hypertension) vs. secondary (10-15% patients) Identifiable causes of hypertension: Pheochromocytoma, renal artery constriction, Cushing s syndrome (hypercorticism) and Cushing s disease (over-production of ACTH), primary aldosteronism, thyroid or parathyroid disease, coarctation of the aorta Pre-existing risk factors and medical conditions (smoking, hyperlipidemia, diabetes, congestive heart failure, asthma, current medications) Individualization (age, gender, ethnicity); patient compliance Single drug (monotherapy) vs. multiple drug (polypharmacy)
9 Development of AHDs - Chronology 1930 Veratrum alkaloids (affect sensitivity of baroreceptors; not currently in use due to toxicity) 1940 Thiocyanates (sodium nitroprusside); ganglion blocking agents (trimethaphan) 1950 Catecholamine depletors (reserpine); vasodilators (hydralazine); PNS sympathetic inhibitors (guanethidine); MAO inhibitors (pargyline); diuretics (hydrochlorothiazides) 1960 CNS α2 agonists (clonidine); beta blockers (propranolol); methyldopa 1970 Alpha1 blockers (prazocin); alpha/beta blockers (labetalol); ACE inhibitors (captopril) 1980 Calcium channel blockers (nimodipine) 1990 Angiotensin-II receptor antagonists (losartan) 2000 Endothelin receptor antagonists (bosentan)
10 Pharmacological mechanism-based classification Diuretics: Thiazide - Hydrochlorothiazide Loop - furosemide, torsemide, ethacrynic acid Potassium-sparing - amiloride, spironolactone, triamterene Sympathoplegic agents: Adrenergic synthesis / release blockers - reserpine, guanethidine Central α-adrenergic agonists α-methyl-dopa, clonidine α blockers - prazosin, tetrazosin, doxazosin β blockers - propranolol, nadolol, timolol, metoprolol, acebutolol, penbutolol, pindolol Ganglion blocker - Trimethaphan Direct vasodilators: hydralazine, minoxidil, sodium nitroprusside, diazoxide Calcium channel blockers: nifedipine, amlodipine, felodipine, diltiazem, verapamil AT-II antagonists & ACE inhibitors: ACE inhbitors captopril, enalapril, enalaprilat, lisinopril, benazepril AT-II receptor antagonists - losartan
11 I. DIURETICS First-line drug for hypertension. Relatively safe and effective. Suitable for older adults. Can be given orally. Use alone or with other antihypertensive agents. Low cost and mostly available in 3 rd world countries. Mechanism of action: Diuretics lower BP by depleting body sodium stores. Full effects take 2 steps: (1) initial reduction of total blood volume and hence cardiac output; peripheral vascular resistance may increase; (2) when CO returns to normal (takes 6-8 weeks), PVR declines.
12 Therapeutic use: Thiazide diuretics, such as hydrochlorothiazide, act on distal convoluted tubule and inhibit Na + -Cl - symport. Can counteract the Na + and H 2 O retention effect of direct vasodilators such as hydralazine and therefore are beneficial for combined use. Particularly useful for elderly patients, but not effective when kidney function is inadequate. Thiazides reduce blood K + and Mg 2+ levels, and induce hypokalemia. It also retains Ca 2+ and decreases urine Ca 2+ content. It is necessary to monitor serum K + level in patients with cardiac arrhythmias and when digitalis is in use.
13 I. DIURETICS Hydrochlorothiazide
14 Loop diuretics, including furosemide, torsemide, and ethacrynic acid, are more powerful than thiazides. They are often used for treatment of severe hypertension when direct vasodilators are administered and Na + and H 2 O retention becomes a problem. Can be used in patients not responding to thiazides. Increase urine Ca 2+ content. Furosemide Devuyst, O. (2008) Nat. Genet., 40,
15 K-sparing diuretics include triamterene, amiloride (both are Na + channel inhibitors), and spironolactone (aldosterone antagonist). Used for treating hypertension in patients who also take digitalis. This class of drugs enhance the natriuretic effects of other diuretics (e.g., thiazides) and counteract the K + depleting effect of these diuretics. Aldosterone Spironolactone
16 Adverse effects and toxicity: (1) Depletion of K + (except K + -sparing diuretics), leading to hypokalemia. (2) Increase uric acid concentration and precipitate gout. (3) Increase serum lipid concentrations. Diuretics are not used for treating hypertension in patients with hyperlipidemia or diabetes. (4) Gynecomastia with spironolactone.
17 II. SYMPATHOPLEGIC AGENTS Centrally acting (on vasomotor center): α-methyldopa, clonidine, guanabenz, guanfacine acting as α2 agonists Blocking synthesis and/or release of NE: reserpine, guanethidine, granadrel Blocking β-adrenoceptors: propranolol, metoprolol, labetalol, etc. Blocking sympathetic ganglia: trimethaphan Blocking α1-adrenoceptors in vessels: prazosin, doxazosin, tetrazosin Blocking renin release: propranolol and other β-blockers
18 CNS Pre-ganglionic Ganglion Post-ganglionic Thoracolumbar Cranial Parasympathetic Sympathetic Sympathetic Sympathetic Ach Nicotinic Ach Nicotinic Ach Nicotinic Ach Nicotinic Ach Muscarinic NE alpha,beta Ach Muscarinic D D1 Cardiac & smooth muscles, gland cells, nerve terminals Cardiac & smooth muscles, gland cells, nerve terminals Sweat glands Renal vascular smooth muscle Sympathetic (adrenal medulla) Ach Nicotinic Epi Released into blood Sacral Motor (somatic) Ach Nicotinic Skeletal muscle Ach = acetylcholine D = dopamine Epi = epinephrine NE = norepinephrine
19 Distribution and functions of AR relating to antihypertensive drug treatment: α1: postsynaptic effector cells, especially smooth muscle Vasoconstriction, relaxation of gastrointestinal smooth muscle, hepatic glycogenolysis α2 presynaptic adrenergic nerve terminals, platelets, lipocytes, smooth muscle Inhibition of transmitter release, platelet aggregation, contraction of smooth muscle β1 postsynaptic effector cells: heart, lipocytes, brain, presynaptic ad./ ch nerve term. Increase cardiac rate & force, relaxation of gastrointestinal smooth muscle β2 postsynaptic effector cells: smooth muscle, cardiac muscle Bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis β3 postsynaptic effector cells: lipocytes Lipolysis
20 Centrally-acting adrenergic drugs: Clonidine A 2-imidazoline derivative that reduces sympathetic and increases parasympathetic tone, leading to BP lowering and bradycardia. Mechanism of action: Clonidine binds α 2 -AR with higher affinity than α 1 -AR. The α 2 -agonistic activity contributes to its BP lowering effect due to negative feedback at the presynaptic neurons. When given i.v., clonidine induces a brief rise of BP, which is followed by prolonged hypotension. In addition, clonidine is thought to bind imidazoline receptors (IR) that have not been fully characterized at molecular level. Similar drugs: guanabenz and guanfacine
21 Therapeutic use: Clonidine reduces CO due to decreased heart rate and relaxation of capacitance vessels. Used for treatment of mild to moderate hypertension, often together with diuretics. Because it decreases renal vascular resistance, it maintains renal blood flow and glomerular filtration and therefore can be used in patients with renal diseases. Clonidine is lipid-soluble and enters brain readily. Half-life is about 8-12 h. Adverse effects and toxicity: Sedation, dry mouth. Clonidine also causes Na + and H 2 O retention. Abrupt withdrawal may induce hypertensive crisis. Do not give to patients who are at risk of mental depression, or are taking tricyclic antidepressants.
22 α-methyldopa α-methyldopa is a prodrug. It enters into adrenergic neurons and is converted by two enzymes to α-methylnorepinephrine, which has the antihypertensive effect. H CH 3 H CH 3 OH CH 3 HO HO C H C COOH NH 2 HO HO C H C NH 2 NH 2 HO HO C H C NH 2 NH 2 α-methyldopa Aromatic L-amino acid decarboxylase α-methyldopamine Dopamine β-oxidase α-methylnorepinephrine Mechanism of action: The metabolite, α-methylnorepinephrine, is stored in neurosecretory vesicle in place of NE. When released, α-methyl-ne is a potent α-ar agonist and in PNS is a vasoconstrictor. Its CNS effect is mediated by α 2 - AR (an autoreceptor), resulting in reduced adrenergic outflow from the CNS and an overall reduced total peripheral resistance.
23 Therapeutic use: This drug does not alter most of the cardiovascular reflexes. Cardiac output and blood flow to vital organs are maintained. It reduces renal vascular resistance and can be used in patients with renal insufficiency. Given orally; effect reaches max. in 4-6 h and continues to 24 h. Not used as first drug in monotherapy, but effective when used with diuretics. Adverse effects and toxicity: Sedation, lassitude, nightmares, lactation (due to inhibition of dopaminergic neuron in hypothalamus). Long-term use may cause development of autoantibodies against Rh locus and give positive Coomb s test.
24 Antihypertensive agents that act on PNS 1. Beta blockers (BBs) Mechanism of action: (1) Reduce cardiac output; (2) inhibit renin release, AT-II and aldosterone production, and lower peripheral resistance; (3) may decrease adrenergic outflow from the CNS. Therapeutic use: Recommended as first-line antihypertensive agents. Combined use with diuretics are common. More effective in treating hypertension in white than in black patients, and in young patients than elderly (due to high occurrence of chronic lung and heart diseases in the elderly). Especially useful in treating hypertension with preexisting conditions such as previous myocardia infarction, angina pectoris, migraine headache. Propranolol: A prototypic β-blocker that antagonizes β 1 and β 2 AR. It inhibits renin production (due to β 1 -antagonistic activity) and can be used in patients with high renin level. It causes no prominent postural hypotension in mild to moderate hypertension patients. This class of drugs also include timolol.
25 Metoprolol: Much less β 2 -antagonistic than propranolol, thus can be used in patients who also suffer from asthma, diabetes, or peripheral vascular disease. Nadolol, carteolol, atenolol, betaxolol, bisoprolol: Slower metabolism and longer half-life for these drugs. They can be administered once daily. The underlined are β 1 -selective antagonists. Pindolol, acebutolol, penbutolol: Antagonistic effect is combined with partial agonistic effect on β 2 -AR. Particularly useful for patients with cardiac failure, bradyarrhythmias, or peripheral vascular disease. Labetalol, carvedilol: These are given as racemic mixture of isomeric compounds. Major advantage is combined α and β blockers and therefore these are more powerful drugs. Labetalol also has some β 2 -agonistic effect. Labetalol is used for treating hypertensive emergencies (injection) or hypertension resulting from pheochromocytoma. Carvedilol can be used in patients with congestive heart failure.
26 Adverse effects and toxicity: (1) Withdrawal syndrome (nervousness, tachycardia, angina, BP increase). (2) Reduced myocardial reserve and peripheral vascular insufficiency; exacerbates asthma, diabetes. (3) Increased plasma triglycerides and decreased HDL cholesterol (propranolol). (4) CNS effects: lassitude, mental depression, insomnia, nightmares. (5) GI effects: diarrhea, constipation, nausea, vomiting.
27 2. Alpha-1 blockers Prazosin, terazosin, doxazosin (all second-line drugs) Mechanism of action: Competitive antagonists for α 1 -AR. Blocking α 1 -AR leads to relaxation of both arterial and venous smooth muscles and thereby reduce PVR. Non-selective alpha blockers: Phentolamine and phenoxybenzamine, for treatment of hypertensive emergencies resulting from pheochromocytoma Therapeutic use: These agents are indirect vasodilators, and are used for treating patients who have not responded to initial antihypertensive therapy. Combined use with propranolol or diuretics may produce additive effects. Long-term use is not likely to cause significant changes in cardiac output and renal blood flow. Thus tachycardia and increased renin release do not occur. No adverse effect on serum lipids and other cardiac risk factors.
28 Adverse effects and toxicity: (1) For prazosin, terazosin, doxazosin: Reflex tachycardia and first-dose syncope are common. Concomitant use with a β-blocker may be necessary. (2) For phentolamine, increased cardiac stimulation (by blocking α 2 -AR negative feedback) can cause severe tachycardia, arrhythmias, and myocardial ischemia. For phenoxybenzamine, postural hypotension may occur. CNS symptoms, such as fatigue, sedation and nausea, are also seen in patients using phenoxybenzamine.
29 3. Ganglion-blocking agents. Not currently used clinically because of toxicity. Trimethaphan: It competitively blocks nicotinic cholinergic receptors on postganglionic neurons, in both sympathetic and parasympathetic ganglia. The antihypertensive effect is due to pooling of blood in capacitance vessels. Antihypertensive effect is rapid, but excessive hypotension may occur. Adverse effects: (1) sympathoplegia (excessive orthostatic hypotension, sexual dysfunction); (2) parasympathoplegia (constipation, urinary retention, dry mouth, precipitation of glaucoma, etc.)
30 Drug Treatment of Hypertension Medical Pharmacology Lecture 42 Marcelo G. Bonini Department of Pharmacology College of Medicine Tel / Room 3035 COMRB
31 4. Agents that block adrenergic neurotransmitter synthesis and/or release. -- Reserpine, guanethidine Reserpine Dopa DD Dopamine Reserpine ATP DBH NE Mechanism of action: Interferes with the Mg 2+ and ATP-dependent uptake of biogenic amines, thereby depleting NE, dopamine, and serotonin. The effect is universal and irreversible. Reserpine acts both centrally and in the periphery. It decreases both CO and PVR.
32 Therapeutic use: Reserpine is effective but has significant adverse effects. It is a 3 rd line AHD. The drug is inexpensive, and the effect stays long even after the drug disappears from circulation. Effective when used at low dose (0.05 mg), in combination with diuretics. Adverse effect and toxicity: Enters brain easily and can produce sedation, mental depression, Parkinson s like symptom. Reserpine should not be given to patients with mental depression or peptic ulcer (for stimulating gastric acid secretion).
33 Guanethidine and guanadrel Mechanism of action: (1) Inhibition of NE release from sympathetic nerve ending. (2) gradual depletion of NE stores in the nerve ending. Guanethidine enters cell through uptake 1, which also recaptures NE. Cocaine and tricyclic antidepressant block uptake 1 and reduce the effect of guanethidine. Na + Tyrosine Deplete NE in vesicle Tyrosine TH Dopa presynaptic DD Dopamine (DA) DBH G ATP G NE (-) G NE α2r Transport blocked by cocaine, TCA Uptake 1 Ca 2+ G = guanethidine NE = norepinephrine Ca 2+ ATP G G G NE NE G G G G Block NE release
34 Therapeutic use: Guanethidine reduces CO due to bradycardia and relaxation of capacitance vessels. Long-term use leads to reduced PVR. Clinically used for outpatient treatment of severe hypertension. Guanethidine is highly basic and cannot enter brain. Therefore there is no CNS adverse effects seen in many other antihypertensive agents. Adverse effects and toxicity: (1) Sodium and water retention are often seen. (2) Postural hypotension and decreased blood flow to heart and brain. (3) Delayed ejaculation in men. Increased GI motility and diarrhea. (4) Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy. Therefore it cannot be used with some over-the-counter cold medicine that contain sympathomimetic agent. Not suitable for patients with pheochromocytoma. (5) Not to be used together with drugs that act on Uptake 1, such as TCA.
35 Direct vasodilators Mechanism of action: These agents relax smooth muscle of arterioles and some also work on veins. They stabilize membrane potential at resting level by opening K + channel (hydralazine, minoxidil, diazoxide), or increase cellular cyclic GMP level which leads to smooth muscle relaxation (sodium nitroprusside).
36 Therapeutic use: The side effects of these AHDs restrict their use in outpatient treatment. They are effective for difficult to control BP. Hydralazine dilates arteries and arterioles. It is used together with a diuretic and a β-blocker, for treatment of moderately severe hypertension. Single-use causes reflex tachycardia and sodium retention. Minoxidil is also used together with a diuretic and a β-blocker, for treatment of severe or malignant hypertension. Diazoxide is used (i.v.) for treating hypertensive emergency. A β-blocker is used together to minimize reflex activation of the heart. Sodium nitroprusside is another drug for hypertensive emergency. It dilates both arteries and veins. Effect takes place immediately (i.v.) but does not last long (1-2 minutes). Thus continuous infusion is required. Adverse effects and toxicity: Reflex tachycardia, sodium retention, and for nitroprusside, cyanide ion production. Minoxidil causes excessive growth of body hair (hypertrichosis) if used for more than 4 weeks. This effect has been used for treating male pattern baldness (Rogaine ).
37 VASODILATING DRUGS Reflex stimulation in response to vasodilating agents PVR Natriuresis Arterial pressure Baroreceptor Sympathetic nervous system outflow Aldosterone Renin release PVR Heart rate, cardiac contractility Venous capacitance Na + retension & plasma volume AT-II Arterial pressure Cardiac output
38 A list of AHDs for treatment of hypertensive emergencies (DBP > 120 mmhg, potentially life-threatening, seen in pheochromocytoma crisis, eclampsia, cocaine overdose, clonidine withdrawal, etc.) Nitroprusside, IV, rapid action (within seconds), short lasting (a few minutes), requires continuous IV infusion. May cause cyanide toxicity. Avoid use in renal failure and pregnancy. Diazoxide, IV, action takes 1-5 min, lasts 4-12 hrs. May cause hyperglycemia, sodium retention, tachycardia. Avoid use in angina pectoris, MI, pulmonary edema, intracranial hemorrhage. Enalaprilat, IV, action seen in 15 min, max in 1-4 hrs, lasts 6-12 hrs. May cause hyperkalemia. Do not use in pregnancy, renal failure in patients with bilateral renal artery stenosis. Hydralazine, IV (action in min) or IM (action in min), lasts 2-6 hrs. May cause angina, tachycardia, headache. Do not use in angina pectoris, MI, aortic dissection. Others: Labetalol, nicardipine, nitroglycerin, trimethaphan, phentolamine.
39 Calcium channel blockers (CCBs) Considered as a different class of vasodilators that are used in treatment of angina and hypertension. Mechanism of action is based on the role of calcium in maintaining smooth muscle tone and in the contraction of myocardium. Blocking the entry of calcium through cell surface L-type channels relaxes smooth muscle cells. Selective blocks arteriole smooth muscle cells is most desirable for reduction of PVR. There are dihydropyridine CCBs and non-dihydropyridine CCBs in treating hypertension. These are alternative drugs for initial treatment of hypertension in patients who cannot take β-blockers (e.g. due to angina + bronchospastic disease). Diphenylalkylamines Verapamil, is less selective on the type of calcium channels and have effects on both arteriole and cardiac SMC. Benzothiazepines -- Diltiazem, has similar function but less adverse effect than verapamil.
40 Dihydropyridines DHPCCBs are an expanding class of CCBs that include amlodipine, nifedipine, felodipine, isradipine, nicardipine, and nisoldipine. They have higher affinity for vascular calcium channels than for cardiac calcium channels. One of these DHPCCBs, amlodipine, is clinically used together with benazepril, an ACE inhibitor, under the commercial name of Lotrel. Amlodipine (Norvasc ) Adverse effects and toxicity: Dizziness, headache and constipation are common. Verapamil should not be used in congestive heart failure patients due to its negative inotropic effect. Use with caution in patients with conductive disturbances involving SA or AV node.
41 ACE inhibitors and angiotensin receptor antagonists: Angiotensinogen Kininogen Renin Kallikrein Angiotensin-I Angiotensin-II ACE (kininase-ii) Bradykinin Inactive products Prostaglandin synthesis John Vane Vasoconstriction Aldosterone secretion Vasodilation PVR BP Na + and H 2 O retension PVR BP ACE = angiotensin-converting enzyme Ervin Erdös
42 ACE inhibitors: Captopril, enalapril, enalaprilat, lisinopril,benazepril, fosinopril, moexipril, quinapril and ramipril Mechanism of action: Captopril and other ACE inhibitors are competitive inhibitors of ACE, mimicking the structure of its substrate. Captopril, enalaprilat and lisinopril are active molecules. Others listed above are prodrugs that need to be converted to active metabolites (di-acids) for functions. ACE inhibitors (1) directly block the formation of AT-II; (2) at the same time increase bradykinin level. The net results are reduced vasoconstriction, reduced sodium and water retension, and increased vasodilation (through bradykinin). Captopril Esterification with EtOH Elanaprilat IV (active) Elanapril (prodrug)
43 Lisinopril, a lysine-analog of enalapril, has several properties that other ACE inhibitors do not have. Lisinopril is hydrophilic, dose not go through liver metabolism and is active (not a prodrug), has good tissue penetration and long half-life (12 hrs), and is excreted unchanged in the urine. Lisinopril is used commonly in the clinic under the commercial names of Zestril and Prinivil. Lisinopril Therapeutic use: First-line alternatives, when diuretics or β-blockers are either ineffective or contraindicated. Most effective in white and young hypertensive patients, or when used together with diuretics. ACE inhibitors are more effective in patients with higher renin level. Commonly used in patients with left ventricular dysfunction (myocardial infarction, chronic congestive heart failure), and also in patients with type I diabetes with renal damage.
44 Adverse effects and toxicity: In hypovolemic patients, severe hypotension may occur after initial doses. Fetotoxic and should not be used in pregnant women. Other adverse effects: Angioedema, dry cough, rashes, altered taste, and proteinuria, and hyperkalemia (especially when used with K + -sparing diuretics).
45 Angiotensin-II receptor antagonists. Losartan (FDA approval in 1995) and valsartan are non-peptide antagonists of AT-II receptor. Other non-peptide antagonists of this class include candesartan, irbesartan, telmisartan (Micardis ), eprosartan, zolasartan and valsartan (Diovan ). These are products of rational drug design. Some of these are in various stages of clinical development. Saralasin is a peptide analog and competitive inhibitor of AT-II receptor, but is orally ineffective and requires continuous intravenous infusion. Saralasin also has partial agonist activity, and is not currently used for hypertension treatment. Mechanism of action: Competitive inhibition of AT-II receptor (Type 1), thereby (1) inhibiting the vasoconstrictor effect of AT-II; (2) prevent the release of aldosterone. Effect is more specific on AT-II action, and less or none on bradykinin production or metabolism.
46 Therapeutic use: Clinical use is similar to ACE inhibitors. Losartan has the advantage of not causing dry cough and angioedema, which are side effects of ACE inhibitors through their bradykinin-increasing action. Adverse effects and toxicity: Similar to those of ACE inhibitors. AT-II antagonists are also fetotoxic and should not be used for treating hypertension in pregnant women.
47 SUMMARY - Mechanisms α-methyldopa, clonidine Reserpine, guanethidine Trimethaphan Propranolol, other β-blockers Thiazide, other diuretics Prazosin, other α1-blockers AT-II receptor antagonists (Losartan) ACE inhibitors (Captopril, Lisinopril, etc) Hydralazine, minoxidil, nitroprusside, diazoxide Calcium channel blockers
48 New antihypertensive drugs Endothelin-1 (ET-1) receptor antagonists. ET-1 is a 21-amino acid peptide present in high concentrations in the lung. At normal (low) concentrations, ET-1 facilitates the relaxation of arterial smooth muscle through its stimulation of prostaglandins and nitric oxide. At high concentrations, such as in the case of pulmonary arterial hypertension, ET-1 activates the two receptors (ETA and ETB) on arterial smooth muscle cells, resulting in vasoconstriction, SMC proliferation and reduction in diameter of arteries. Bosentan, also known as Tracleer, is a dual receptor antagonist which blocks both ETA and ETB. Bosentan is orally effective. In a trial of 12 weeks, pulmonary hemodynamic measurements revealed decreases in pulmonary arterial pressure and pulmonary vascular resistance and increase in cardiac output in patients given bosentan, compared with worsening of pulmonary hemodynamics in patients receiving placebo. Side effects include liver toxicity (increase in transaminase) and fetal toxicity.
49 AHD type Diuretics (hydrochlorothiazide, furosemide, ethacrynic acid, torsemide) β-blockers (propranonol, metoprolol, pindolol, timolol) ACE inhibitors (Captopril, lisinopril, enalapril, enalaprilat) Angiotensin receptor blockers (Losartan) Mechanisms of action, benefits and potentially unfavorable effects Natriuresis, PVR. Well tolerated, can be given orally, once a day, effective for elderly and black patients, inexpensive. Osteoporosis CO, renin level, NE release Atrial tachyarrhythmias/fibrillation, essential tremor, thyrotoxicosis Ang II formation, vasoconstriction, aldosterone secretion, Improves kidney blood flow, less metabolic effects Competitively block Ang II type I receptor, Same benefits as ACEI, but no dry cough Side effects and toxicity Hypokalemia, hyperuricemia, hyperglycemia, hypercholesterolemia, hyponatremia, gout Bradycardia, altered lipids and glucose levels, Bronchoconstriction (β2 blockers) Teratogenic effects, angioedema, hyperkalemia, dry cough Teratogenic effects, possible hypokalemia Aldosterone antagonists (K + -sparing diuretics) (spironolactone, ) Block aldosterone receptor, Inhibits sodium and water retention, inhibits vasoconstriction Hyperkalemia, hyponatremia, gynecomastia (spironolactone)
50 AHD type Action mechanism and benefits Side effects and toxicity Calcium channel blockers (DHPCCBs, verapamil, diltiazem) α1 blockers (prazosin, tetrazosin doxazosin) Reduce calcium entry into SMC, resulting in coronary and peripheral vasodilation Vasodilation through inhibition of α1 adrenergic receptor Reflex tachycardia, flushing, peripheral edema, non-dhpccb blocks AV node Hypotension, first dose syncope Central α2 agonists (α-methydopa, clonidine) Blcker for NE synthesis and release (reserpine, guanethidine) Direct vasodilators (hydralazine, minoxidil, sodium nitroprusside) Stimulate inhibitory neurons in vasomotor centers, reduce sympathetic outflow from CNS, Reduce both CO and PVR Deplete catecholamine from storage granules. Once a day, low cost, third line AHDs Rapid effect, especially for difficult to control BP Anticholinergic side efffects: sedation, dizziness, dry mouth fatigue. Increase fluid retention (+ diuretics) Fluid retention for reserpine Reflex cachycardia, fluid retention
51 Recommended AHDs with compelling indications Compelling indication Diuretic Betablocker ACEI ARB CCB Aldosterone antagonist Heart failure Post-MI High coronary disease risk Diabetes Chronic kidney disease Recurrent stroke prevention
52 SUMMARY - Treatment First-line drugs for monotherapy: (1) Thiazide diuretics. (2) beta blockers. Alternative first-line drugs: ACE inhibitors, calcium channel blockers, selective α1-blockers (prazosin), α + β blockers (labetalol) Drugs not preferred for monotherapy: Hydralazine, minoxidil Combined use of 2 drugs: (1) Diuretic + β-blocker (2) Diuretic + ACE inhibitor (3) ACE inhibitor + calcium channel blocker (4) AT-II receptor blocker + diuretic Combined use of 3 drugs: (1) Diuretic + sympathoplegic agent + direct vasodilator (2) Diuretic + ACE inhibitor + direct vasodilator
53 In case of concomitant diseases: Angina pectoris: Congest. heart failure: Previous MI: Diabetes (IDDM): Hyperlipidemia: Asthma, chronic pulmonary disease: β-blockers, calcium channel blockers (alternatively, diuretics, ACE inhibitors) Diuretics, ACE inhibitors (No verapamil; no β-blockers) β-blockers, ACE inhibitors Alternatively, diuretics, calcium channel blockers ACE inhibitors, calcium channel blockers, α-blockers (No diuretics, no β-blockers) ACE inhibitors, calcium channel blockers (No diuretics, no β-blockers) Diuretics, calcium channel blockers (No β 2 -blockers)
54 Drug treatment of hypertension -- indications: Elderly, African-American patients: Diuretics, long-acting calcium channel blockers Young, caucasian patients: β-blockers, ACE inhibitors, AT-II receptor blockers Obesity: Diuretics Drug treatment of hypertension -- countraindications: Pregnancy: Congest. Heart failure: ACE inhibitors, AT-II receptor blockers Verapamil Treatment of hypertensive emergencies: Vasodilators (sodium nitroprusside, diazoxide, hydralazine) Calcium channel blockers, reserpine, methyldopa, labetalol
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