Downloaded 74 times
More Related Content
Similar to Directly acting vasodilators
Directly acting vasodilators
- 1.
- 2. Directly Acting Vasodilators Classification A-Accordingto route of adminstration 1-Oral Vasodilators Hydralazine Minoxidil 2-Parenteral Vasodilators Sodium Nitroprusside Diazoxide Fenoldopam 3-Oral & Parenteral Vasodilators Calcium Channel Blockers
- 3. Drugs Used Parenterallyare for hypertensive emergencies Among these only Na Nitroprusside is both Arteriolar and Venous Dilators while all the others are arterial dilators
- 4. Vasodilator Decreased PVR Decreased BP Activationof Renin-Angiotensin-System Activation of BaroreceptorSympathetic System Increased Renin Release Increased HR, FOC Angitensinogen__Angiotensin-1 Increased C O -------- Increased B.P Angiotensin-2 Reflex Tachycardia prevented by Beta-Blockers Increased Aldosterone Increased Na+ & Water Retension Increased Blood Volume Increased B.P
- 5. So Vasodilators tendto: 1. Increase BP back to high levels by a) Increasing Renin Release b) Increasing Sympathetic outflow through the baroreceptor reflex 2. Cause Reflex Tachycardia (Again increased reflex sympathetic activity
- 6. Other Common Features 1.Most can cause Palpitations and can precipitate angina and arrythmias due to the increased sympathetic activity (However these effects are less or absent with Calcium Channel Blockers due to their depressant effects on the heart)
- 7. 2. They alsocause headache and flushing due to the vasodilatation 3. They may also cause salt and water retention (Increased Renin and aldosterone) and thus edema 4. They do not cause postural Hypotension because sympathetic reflexes are intact
- 8. Common Use: Hypertension Bycausing vasodilatation they decrease PVR. Not used alone because of the compensatory mechanisms causing various adverse effects Used with Beta Blockers to decrease the effects on heart due to reflex increase in sympathetic activity And used with diuretics to decrease the plasma volume increased due to retention of Na and increased renin and aldosterone
- 9. Hydralazine Given orally, Metabolisedby Acetylation Mechanism of Action Not clear; It may involve generation of NO and stimulation of cGMP Uses Hypertension CCF (Decreases Afterload)
- 11. Adverse Effects ofHydralazine All the common adverse effects: (Extension of pharmacological effects) Tachycardia, palpitations leading to angina and arrythmias Hypotension Headache and flushing
- 12. Distinctive Adverse Effect(immunological) Mechanism is unknown 1-SLE like syndrome—high doses or slow acetylators—arthralgia, myalgia, skin rashes and fever 2-Illness resemble Serum Sickness Haemolytic Anaemia Vasculititis Glomerulonrphritis 3—Pyridoxine responsive polyneuropathy Other adverse Effects Anorexia, nausea, sweating
- 13. Minoxidil Orally given andconverted into active form in body---Minoxidil Sulfate, Only dilates arerioles
- 14. Mechanism of Action It is a Potassium Channel opener Relaxation of vascular smooth muscle by activation of ATP-Modulated K+ Channels. By opening K+ Channels----- increased K+ Efflux This results in hyperpolarisation and stabilizes the membrane at its resting potential------ Relaxation of vascular smooth muscle ------- Vasodilation ------ decreased PVR -------decreased B.P
- 15. Uses: Hypertension Severe, lifethreatening,drug resistant Alopecia Used to stimulate hair growth in male pattern baldness (Topical therapy)
- 16. Mechanism of increasehair growth Exact is unknown but may involve; a.Increase microcirculation around hair follicles. b.Direct stimulation of resting hair follicles. c.Alteration of androgen effect on genetically hair follicles.
- 17. Adverse Effect Oedema Reflex tachycardia Hypotension Rashes, Steven Johnson’s syndrome Glucose intolerance Thrombocytopenia Distinctive Adverse Effect Hirsutism (Hence used for baldness)
- 18. Diazoxide Given Parenterally, arteriolardilator Structural similarity to Thiazide diuretics but no diuresis Mechanism of Action Potassium channel Opener like Minoxidil
- 19. Distinctive Adverse Effects Extensive Hypotension Hyperglycemia (Inhibits insulin release from pancreas by opening potassium channels in the Beta cells of pancreas and hence used in treatment of insulinoma Gout Hirsutism Pain & necrosis on extavasation
- 20. Uses Hypertensive crisis Hyperinsulinaemia Eclampsia Alopecia Preterm labour
- 21. Sodium Nitroprusside Parenterally Administered;Arterial and Venous Dilator Mechanism of Action It causes release of Nitric oxide that activates guanylyl cyclase or it may directly stimulate the enzyme to increase cGMP which relaxes vascular smooth muscle
- 22. Uses Hypertensive Emergencies Heart Failure DistinctiveAdverse Effects Cyanide Poisoning: Nitroprusside is a complex of iron, cyanide and a nitroso group and is rapidly metabolized by uptake into RBCs with liberation of cyanide
- 23. Most of thecyanide is converted into thiocyanate which is less toxic and slowly excreted through kidneys Accumulation of cyanide causes: Metabolic acidosis, arrythmias, excessive hypotension and death Treatment: Give sodium thiosulfate to convert to thiocyanate or give hydrxocobalamin that forms non toxic cyanocobalamin
- 24. Thiocyanate may accumulateand cause weakness, disorientation, psychosis, muscle spasms, and convulsions and hypothyroidism Na Nitroprusside may also cause Methemoglobinemia delayed hypothyroidism.
- 25. Fenoldopam New Parenteral arteriolardilator Mechanism of Action D1 receptor agonist resulting in dilatation of peripheral arteries and natriuresis Distinctive Adverse Effect Increases Intraocular pressure and thus avoided in glaucoma