Vasodilators

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Information about Vasodilators

Published on January 30, 2009

Author: hafsamaryam

Source: slideshare.net

TOPIC OF PRESENTATION: “ VASODILATORS” PRESENTED BY: HAFSA MARYAM ROLL NO. 11

VASODILATORS: Agents that act as blood vessel dilators. These act by producing relaxation of the vascular smooth muscle, which decrease peripheral vascular resistance and therefore blood pressure.

Agents that act as blood vessel dilators. These act by producing relaxation of the vascular smooth muscle, which decrease peripheral vascular resistance and therefore blood pressure.

DIRECT-ACTING VASODILATORS FENOLDOPAM PARENTRAL HYDRALAZINE ORAL MINOXIDIL ORAL SODIUM NITROPRUSSIDE PARENTRAL DIAZOXIDE PARENTRAL

FENOLDOPAM

PARENTRAL

Increased sympathetic system outflow. This leads to: Increased heart rate Increased cardiac contractility Decreased venous capacitance Increased cardiac output. VASODILATOR DRUGS Decreased systemic vascular resistance. Decreased arterial pressure. Increased renin release. Increased angiotensin II. Decreased renal sodium excretion. Sodium retention, increased plasma volume Increased systemic vascular resistance. Increased arterial pressure Increased aldosterone COMPENSATORY RESPONSES TO VASODILATORS

Increased sympathetic system outflow.

This leads to:

Increased heart rate

Increased cardiac contractility

Decreased venous capacitance

Increased cardiac output.

VASODILATOR DRUGS

Decreased systemic vascular resistance.

Decreased arterial pressure.

Increased renin release.

Increased angiotensin II.

Increased systemic vascular resistance.

Increased arterial pressure

The direct-acting vasodilator used clinically is Hydralazine (Apresoline) HYDRALAZINE

` Oral vasodilator but can be given I/V. Well absorbed. Rapidly metabolized by the liver during first pass so bioavailability is low averaging 25% variable among individuals. It is also metabolized in part by acetylation. 40 mg/d to 200 mg/d. PHARMACOKINETICS OF HYDRALAZINE DOSE: Risk of toxicity is increased in slow acetylators. Rapid acetylators require higher doses.

Oral vasodilator but can be given I/V.

Well absorbed.

Rapidly metabolized by the liver during first pass so bioavailability is

low averaging 25%

variable among individuals.

It is also metabolized in part by acetylation.

40 mg/d to 200 mg/d.

Risk of toxicity is

increased in slow

acetylators.

Rapid acetylators

require higher

doses.

PHARMACODYNAMICS OF HYDRALAZINE Opens k+ channels and relaxes the smooth muscles of arterioles. This leads to decrease in peripheral vascular resistances. Decrease in arterial blood pressure. It causes reflex stimulation of sympathetic system. This leads to increased heart rate Increased myocardial contractility Increased cardiac output Increased plasma renin activity Increased fluid retention. This leads to increased arterial pressure and thus antagonizes its antihypertensive action. It is thus given with A Beta blocker A diuretic. VASODILATION: COMPENASTORY RESPONSE:

Opens k+ channels and relaxes the smooth muscles of arterioles.

This leads to decrease in peripheral vascular resistances.

Decrease in arterial blood pressure.

It causes reflex stimulation of sympathetic system. This leads to

increased heart rate

Increased myocardial contractility

Increased cardiac output

Increased plasma renin activity

Increased fluid retention.

This leads to increased arterial pressure and thus antagonizes its antihypertensive action.

It is thus given with

A Beta blocker

A diuretic.

Moderate to severe hypertension Hypertensive emergency Heart failure. Hydralazine monotherapy is used in treatment of pregnancy induced hypertension. Ischemic heart disease Lupus erythematosus INDICATIONS OF HYDRALAZINE: CONTRA-INDICATIONS OF HYDRALAZINE:

Moderate to severe hypertension

Hypertensive emergency

Heart failure.

Hydralazine monotherapy is used in treatment of pregnancy induced hypertension.

Ischemic heart disease

Lupus erythematosus

ADVERSE EFFECTS OF HYDRALAZINE CNS: Headache Dizziness Peripheral neuropathy CVS: Palpitation Flushing Reflex tachycardia Angina Ischemic arrhythmias GIT: Anorexia Nausea. SKIN: Sweating Lupus erythematosus like syndrome characterized by: Arthralgia Myalgia Skin rashes fever

CNS:

Headache

Dizziness

Peripheral neuropathy

CVS:

Palpitation

Flushing

Reflex tachycardia

Angina

Ischemic arrhythmias

GIT:

Anorexia

Nausea.

SKIN:

Sweating

Lupus erythematosus like syndrome characterized by:

Arthralgia

Myalgia

Skin rashes

fever

MINOXIDIL

It is prodrug. Administered orally but can be applied topically. 90% absorption from gastrointestinal tract. Topical minoxidil is poorly absorbed averaging 2%. It is widely distributed in body tissues. Plasma half life is 4 hrs. Metabolized in the liver by the process of conjugation forming its sulfates. Action is due to its active metabolite minoxidil sulphate. It is excreted mainly by the kidneys. 5-40mg/d in single or divided doses. PAHARMACOKINETICS OF MINOXIDIL: DOSE:

It is prodrug.

Administered orally but can be applied topically.

90% absorption from gastrointestinal tract.

Topical minoxidil is poorly absorbed averaging 2%.

It is widely distributed in body tissues.

Plasma half life is 4 hrs.

Metabolized in the liver by the process of conjugation forming its sulfates.

Action is due to its active metabolite minoxidil sulphate.

It is excreted mainly by the kidneys.

5-40mg/d in single or divided doses.

Due to reflex tachycardia it is given along with a diuretic and Beta blocker. Opens k+ channels in smooth muscles of arterioles. Hyperpolarization of smooth muscles leading to dilation of blood vessels. Decrease in peripheral vascular resistance. Decrease in blood pressure. OF MINOXIDIL: PHARMACODYNAMICS IT CAUSES VASODILATON BY THE FOLLOWING MECHANISM:

Due to reflex tachycardia it is given along with a diuretic and Beta blocker.

Opens k+ channels in smooth muscles of arterioles.

Hyperpolarization of smooth muscles leading to dilation of blood vessels.

Decrease in peripheral vascular resistance.

Decrease in blood pressure.

Severe hypertension Severe hypertension coupled with renal function impairment. Topical use for correction of baldness in males OF MINOXIDIL: INDICATIONS

Severe hypertension

Severe hypertension coupled with renal function impairment.

Topical use for correction of baldness in males

CNS: Headache. CVS: Tachycardia Palpitation Angina Pericardial effusion. SKIN: Sweating Flushing. ENDO: Hirsuitism (hypertrichosis) in females. RENAL: Edema. OF MINOXIDIL: ADVERSE EFFECTS

CNS:

Headache.

CVS:

Tachycardia

Palpitation

Angina

Pericardial effusion.

SKIN:

Sweating

Flushing.

ENDO:

Hirsuitism (hypertrichosis) in

females.

RENAL:

Edema.

It is an effective and relatively long-acting parentral vasodilator. It has thiazide diuretic like action but no diuretic effects. It is a parentral direct acting vasodilator. DIAZOXIDE:

It is an effective and relatively long-acting parentral vasodilator.

It has thiazide diuretic like action but no diuretic effects.

It is a parentral direct acting vasodilator.

It is administered parentrally. It is bound extensively to serum albumin. Its is both metabolized and excreted unchanged. Its metabolic pathways are not well characterized. Its half life is about 24 hours The blood pressure lowering effect of diazoxide is established within 5 min and lasts for 4-12 hours. Treatment should be started with low doses about 50 to 150mg. Dose of 150 mg should be increased after every 5 min until BP is lowered. PHARMACOKINETICS OF DOSE:

It is administered parentrally.

It is bound extensively to serum albumin.

Its is both metabolized and excreted unchanged.

Its metabolic pathways are not well characterized.

Its half life is about 24 hours

The blood pressure lowering effect of diazoxide is established within 5 min and lasts for 4-12 hours.

Treatment should be started with low doses about 50 to 150mg.

Dose of 150 mg should be increased after every 5 min until BP is lowered.

It causes vasodilation by: Opening k+ channels in the smooth muscles of arterioles thus relaxing them. This decreases peripheral vascular resistance. Decreased arterial blood pressure. Reflex sympathetic system stimulation. It also relaxes smooth muscles other than the vascular ones. It inhibits the release of insulin from beta cells of pancreas thus leading to hyperglycemia. OF DIAZOXIDE:

It causes vasodilation by:

Opening k+ channels in the smooth muscles of arterioles thus relaxing them.

This decreases peripheral vascular resistance.

Decreased arterial blood pressure.

Reflex sympathetic system stimulation.

It also relaxes smooth muscles other than the vascular ones.

It inhibits the release of insulin from beta cells of pancreas thus leading to hyperglycemia.

I/V in hypertensive emergencies. Orally in hypoglycemia caused by hyperinsulinemia. Diabetes mellitus Congestive cardiac failure. INDICATIONS OF DIAZOXIDE: CONTRA-INDICATIONS OF DIAZOXIDE:

I/V in hypertensive emergencies.

Orally in hypoglycemia caused by hyperinsulinemia.

Diabetes mellitus

Congestive cardiac failure.

CVS: Severe hypotension resulting in stroke or myocardial infarction. Angina Cardiac failure in pts with ischemic heart disease. ENDO: Hyperglycemia RENAL: edema ADVERSE EFFECTS OF DIAZOXIDE:

CVS:

Severe hypotension resulting in stroke or myocardial infarction.

Angina

Cardiac failure in pts with ischemic heart disease.

ENDO:

Hyperglycemia

RENAL:

edema

SODIUM NITROPRUSSIDE

It is administered parentrally by continuous I/V infusion. It is poisonous if given orally because of hydrolysis into cyanide. It is taken up and metabolized by RBCs with liberation of cyanide. Mitochondrial enzyme rhodanase in the presence of a sulfur donor metabolizes it to less toxic thiocyanate. Thiocyanate is distributed in ECF and eliminated by the kidneys. Dosage typically begins at 0.5ug/kg/min. It may be increased up to 10ug/kg/min as necessary to control blood pressure. PHARMACOKINETICS OF Na NITROPRUSSIDE: DOSE:

It is administered parentrally by continuous I/V infusion.

It is poisonous if given orally because of hydrolysis into cyanide.

It is taken up and metabolized by RBCs with liberation of cyanide.

Mitochondrial enzyme rhodanase in the presence of a sulfur donor metabolizes it to less toxic thiocyanate.

Thiocyanate is distributed in ECF and eliminated by the kidneys.

Dosage typically begins at 0.5ug/kg/min.

It may be increased up to 10ug/kg/min as necessary to control blood pressure.

It dilates both arterial and venous vessels. Its action is due to nitric oxide. Nitric oxide of sodium nitroprusside. Activation of guanylyl cyclase (GC) in smooth muscles of blood vessels. Increased intracellular cGMP. Relaxation of vascular smooth muscle. PHARMACODYNAMICS OF Na NITROPRUSSIDE:

It dilates both arterial and venous vessels.

Its action is due to nitric oxide.

Nitric oxide of sodium nitroprusside.

Activation of guanylyl cyclase (GC) in smooth muscles of blood vessels.

Increased intracellular cGMP.

Relaxation of vascular smooth muscle.

CVS: Directly relaxes both arterial and venous smooth muscles equally Decreases BP in supine and upright position. Decreases myocardial oxygen demand due to increased venous capacitance. Slight increase in heart rate and decrease in cardiac output except in cardiac failure. In cardiac failure it may decrease heart rate and increase cardiac output. RENAL: Renal blood flow is maintained and renin secretion is increased. EFFECTS OF Na NITROPRUSSIDE:

CVS:

Directly relaxes both arterial and venous smooth muscles equally

Decreases BP in supine and upright position.

Decreases myocardial oxygen demand due to increased venous capacitance.

Slight increase in heart rate and decrease in cardiac output except in cardiac failure.

In cardiac failure it may decrease heart rate and increase cardiac output.

RENAL:

Renal blood flow is maintained and renin secretion is increased.

Hypertensive crisis Heart failure Cardiac surgery to produce hypotension Cardiogenic shock Aortic dissection Regurgitant valvular disease. INDICATIONS OF Na NITROPRUSSIDE:

Hypertensive crisis

Heart failure

Cardiac surgery to produce hypotension

Cardiogenic shock

Aortic dissection

Regurgitant valvular disease.

Cyanide toxicity: Metabolic acidosis Excessive hypotension Arrhythmias death BLOOD: Methemoglobinemia THIOCYANATE POISONING: Weakness Disorientation Psychosis Muscle spasms Convulsions. ENDO: Delayed hypothyroidism ADVERSE EFFECTS OF Na NITROPRUSSIDE:

Cyanide toxicity:

Metabolic acidosis

Excessive hypotension

Arrhythmias

death

BLOOD:

Methemoglobinemia

THIOCYANATE POISONING:

Weakness

Disorientation

Psychosis

Muscle spasms

Convulsions.

ENDO:

Delayed hypothyroidism

Thank You

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