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HYPERTENSION

HYPERTENSION. Sustained hypertension can damage blood vessels in kidney, brain and heart = incidence of renal failure, cardiac failure and stroke. Normal BP control mechanisms. Renin –angiotensin –aldosterone system Baroreceptor reflex. Stage. Diastolic Range (mm Hg). Systolic Range (mm Hg).

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HYPERTENSION

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  1. HYPERTENSION

  2. Sustained hypertension can damage blood vessels in kidney, brain and heart = incidence of renal failure, cardiac failure and stroke

  3. Normal BP control mechanisms • Renin –angiotensin –aldosterone system • Baroreceptor reflex

  4. Stage Diastolic Range (mm Hg) Systolic Range (mm Hg) High Normal 85-89 130-139 Stage 1 90-99 140-159 Stage 2 100-109 160-179 Stage 3 > 109 >179

  5. Na+ Na+ Drugs acting on therenin-angiotensin system. arteries Angiotensinogen AI AII Renin adrenal glands Aldosterone kidneys

  6. Drugs acting on therenin-angiotensin system arteries Angiotensinogen AI AII Renin adrenal glands Aldosterone kidneys Na+ Na+

  7. ACE Inhibitors AIIRA Calcium Blockers Diuretics Beta-blockers Spironolactone Drugs acting on therenin-angiotensin system. arteries Angiotensinogen AI AII Renin adrenal glands Aldosterone kidneys

  8. Diuretics • Thiazides, loop diuretics, potassium sparing diuretics

  9. ACE inhibitors/ ARB • Captopril, enalapril, ramipril, lisinopril • Losartan, valsartan, irbesartan

  10. Beta blockers • Atenolol, metaprolol, carvedilol, labetalol

  11. Calcium channel blockers • Verapamil, diltiazem, nifedipine, amlodipine

  12. a-blockers • Mechanism of action: blockade of vascular a -adrenoceptors • Non selective (a1 and a2) blockers: Phentolamine, phenoxybenzamine and dibenamine • Selective (a1: prazosin,terazosin, doxazosin, trimazosin)

  13. Hydralazine • Direct acting vasodilator: liberates NO from vascular endothelium which stimulates the production of cGMP in vascular smooth muscle, resulting in relaxation (arterioles > veins) • Can NOT be used for monotherapy • Tachycardia with palpitations, hypotension , nausea, vomiting, sweating, Lupus erythmatosis • Never use as first choice; Try in refractory hypertension as part of a multidrug regimen

  14. Minoxidil • Prodrug of minoxidil sulfate, which is a direct acting vasodilator • Mechanism: K+ channel opener, causes membrane hyperpolarization, reducing ability of smooth muscle to contract. • Other K channel openers: pinacidil, diazoxide • refractory hypertension • Long duration of action (>24 hours)

  15. Minoxidil Adverse Effects • Fluid and water retention: can lead to pulmonary hypertension • Tachycardia and increased cardiac output: • Headache, sweating, hirsutism

  16. DIAZOXIDE • occasionally - hypertensive emergencies. • opening potassium channels • half-life; 24 hours, rapid injection onset 5 minutes lasts 4-12 hours • hypotension→ stroke and myocardial infarction / provoke angina, cardiac failure in patients with ischemic heart disease → when dose of 300 mg is used; instead infuse at 15-30 mg/min • avoided in IHD • inhibits insulin release → used to treat hypoglycemia secondary toinsulinoma

  17. SODIUM NITROPRUSSIDE • hypertensive emergencies as well as severe heart failure • dilates both arterial and venousvessels, ↓ PVR & venous return - cardiac output decreases • activation of guanylylcyclase -relaxesvascular smooth muscle • In heart failure and low cardiac output, output often increases owing to afterload reduction

  18. Rapid & short acting 1- 10 minutes on discontinuation - IV infusion • Metabolic acidosis, arrhythmias, hypotension • methemoglobunemia

  19. FENOLDOPAM • D1 agonist peripheral arteries and natriuresis= hypertensive emergencies and postoperative hypertension. • rapidly metabolized conjugation half-life 10 minutes continuous intravenous infusion. • Reflex tachycardia, flushing, headache increases intraocular pressureavoid in glaucoma

  20. Centrally Acting Sympatholytics:a2-Adrenoceptor Agonists • a-Methyldopa • Clonidine

  21. a2-Adrenoceptor Agonists Mechanisms of Action • Central Action: Stimulation of a2 adrenoceptors in the brainstem reduces sympathetic tone, causing a centrally mediated vasodilatation and reduction in heart rate • Prejunctional action: Stimulation of a2 adrenoceptors located prejunctionally on peripheral neurons reduces norepinephrine release

  22. Clonidine • Partial agonist - a2A • Lipid soluble, short half life. • Dry mouth, sedation, salt & water retention, hypotension, • Sudden withdrawal = hypertensive crises • Moderately potent antihypertensive

  23. Methyldopa • Mild to moderately severe HT • ↓ PVR, ↓ CO & HR, ↓ renal vascular resistance. • Sedation, orthostatic hypertension, impaired mental conc. , lactation, nightmares, mental depression, fluid retention.

  24. Reserpine Molecular mechanism of action: Inhibition of noradrenergic function. • Interferes with uptake mechanism, Storage vesicles are destroyed and nerve ending loses capacity to store and release norepinephrine and serotonin • Pharmacological consequences: reduction of cardiac output and TPR

  25. Reserpine • Extremely long acting • Mild to moderate HT • Postural hypotension, diarrhoea, abdominal cramps • CNS effects: • Sedation, loss of concentration • psychotic depression. • Extrapyramidal effects

  26. Guanithidine • Sympathoplegic • Inhibits release release of NA from sympathetic nerve ending. • Long half life (5 days) • Hypotension, diarrhoea, delayed or retrograde ejaculation

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