It directly causes relaxation of the peripheral vessels.
Mechanism of action:
It causes the release of nitric oxide (NO). NO is a relaxing factor. NO stimulates guanylyl cyclase in vascular smooth muscle leading to vasodilatation.
When it acts on arterioles it causes a reduction in total systemic vascular resistance leading to a fall in blood pressure.
Actions:
It causes relaxation of smooth muscles of both arteries and veins resulting in the immediate vasodilatation with reflex tachycardia.
Cardiac rate is promoted in the supine position and reduced in the standing position. Cardiac rate is increased reflexly.
It results in reduced oxygen demand of the heart muscles caused by promoted venous capacitance.
It regulates the blood to the kidneys and there is a slightly promoted renin secretion.
Pharmacokinetics:
It is rapidly metabolized as its half life is about 2 minutes. Its metabolism causes the production of cyanide ions. It is eliminated by the kidney.
Therapeutic uses:
1. It is used in hypertensive crisis as it has the ability of reducing the blood pressure in standing as well as supine position.
2. It is used for reducing bleeding during surgery
3. It is used in ventricular unloading in acute congestive heart failure.
4. It is used for acute myocardial infarction
Adverse effects:
It may cause headache, excessive hypotension, tachycardia, agitation, palpitation, restlessness, nausea, cyanide ions poisoning (which can be treated by using sodium thiosulfate), disorientation, muscle spasms and convulsions.
Dosage and administration:
It is given by continuous IV infusion in the dose of 0.5-1.0 μg/kg/min.
Saturday, April 9, 2011
Diazeoxide
It is a benzothiazide.
Mechanism of action:
Diazoxide causes activation of the ATPase sensitive potassium channels resulting in the hyperpolarization of the vascular smooth muscles leading to the relaxation of the arterioles (smooth muscles) leading to reduced systemic vascular resistance resulting in diminished blood pressure.
It causes a promoted cardiac rate and cardiac output along with a fall in both of the systolic and diastolic pressure due to its vasodepressive action. This vasodepression is most importantly due to arteriolar dilatation, however venous dilatation is also effective in causing vasodepression.
It also causes relaxation of the other smooth muscles.
It also blocks the release of insulin from pancreatic β-cells. It can cause salt and water retention resulting in weight gain.
Therapeutic uses:
1. It is used in hypertensive crisis (IV).
2. It is used in hypoglycemia due to hyperinsulinemia (Oral).
Pharmacokinetics:
Most of the drug gets bind with protein. Its plasma half life is about 25-60 hours. The drug is eliminated by renal tubular secretion and biotransformation.
Adverse effect:
It may cause Angina, edema, serious hypotension which may lead to stroke and myocardial infarction or Hyperglycemia.
Contraindications:
It is contraindicated in patients of
1. Diabetes mellitus
2. Congestive heart failure
Dosage:
In the beginning 75-100 mg; but if necessary dose may increase up to 150 mg every 5 minute until blood pressure comes to normal.
Mechanism of action:
Diazoxide causes activation of the ATPase sensitive potassium channels resulting in the hyperpolarization of the vascular smooth muscles leading to the relaxation of the arterioles (smooth muscles) leading to reduced systemic vascular resistance resulting in diminished blood pressure.
Actions:
It causes a promoted cardiac rate and cardiac output along with a fall in both of the systolic and diastolic pressure due to its vasodepressive action. This vasodepression is most importantly due to arteriolar dilatation, however venous dilatation is also effective in causing vasodepression.
It also causes relaxation of the other smooth muscles.
It also blocks the release of insulin from pancreatic β-cells. It can cause salt and water retention resulting in weight gain.
Therapeutic uses:
1. It is used in hypertensive crisis (IV).
2. It is used in hypoglycemia due to hyperinsulinemia (Oral).
Pharmacokinetics:
Most of the drug gets bind with protein. Its plasma half life is about 25-60 hours. The drug is eliminated by renal tubular secretion and biotransformation.
Adverse effect:
It may cause Angina, edema, serious hypotension which may lead to stroke and myocardial infarction or Hyperglycemia.
Contraindications:
It is contraindicated in patients of
1. Diabetes mellitus
2. Congestive heart failure
Dosage:
In the beginning 75-100 mg; but if necessary dose may increase up to 150 mg every 5 minute until blood pressure comes to normal.
Guanethidine
Mechanism of action:
Its neurotransmission is almost similar to the process of norepinephrine.
It replaces norepinephrine in the transmitter vesicles resulting in the reduction of norepinephrine in the nerve endings. This causes the inhibition of the release of norepinephrine from the sympathetic nerve endings.
Actions:
As it causes the replacement of norepinephrine, so firstly, mild cardiac stimulation and minor form of hypertension that lasts for short duration, occurs.
This is followed by bradycardia and hypotension (orthostatic type of hypotension occurs mostly as it decreases vasoconstrictor reflexes.)
It promotes tissues sensitivity to catecholamines.
Therapeutic uses::
In combination with diuretic and vasodilator it can be used for moderate to severe type of hypertension.
Adverse effects:
Weakness, Orthostatic hypotension, Diarrhea
Contraindications:
It is contraindicated in patients of
1. Pheochromocytoma
2. Serious coronary artery disease
3. Cerebrovascular insufficiency
4. While using MAO inhibitors
Its neurotransmission is almost similar to the process of norepinephrine.
It replaces norepinephrine in the transmitter vesicles resulting in the reduction of norepinephrine in the nerve endings. This causes the inhibition of the release of norepinephrine from the sympathetic nerve endings.
Actions:
As it causes the replacement of norepinephrine, so firstly, mild cardiac stimulation and minor form of hypertension that lasts for short duration, occurs.
This is followed by bradycardia and hypotension (orthostatic type of hypotension occurs mostly as it decreases vasoconstrictor reflexes.)
It promotes tissues sensitivity to catecholamines.
Therapeutic uses::
In combination with diuretic and vasodilator it can be used for moderate to severe type of hypertension.
Adverse effects:
Weakness, Orthostatic hypotension, Diarrhea
Contraindications:
It is contraindicated in patients of
1. Pheochromocytoma
2. Serious coronary artery disease
3. Cerebrovascular insufficiency
4. While using MAO inhibitors
Reserpine
It is a plant alkaloid derived from the roots of plant Rauwolfia Serpentina.
Mechanism of action:
Reserpine works to prevent neuronal and chromaffin granule transporters by Mg2+/ATP dependent transport mechanism.
As a consequence accumulation of catecholamine transmitters by adrenergic transmitter vesicles is prevented resulting in great depletion of transmitters in both central and peripheral neurons that can remain for days to weeks. Monoamine oxidase has the ability of degrading norepinephrine in the cytoplasm.
It also exerts a direct vasodilating effect on vascular smooth muscles when administered intra-arterially.
Actions:
1. It causes sedation due to depletion of biogenic amines centrally.
2. It decreases cardiac rate, cardiac output and blood pressure.
3. It may also decrease peripheral vascular resistance.
4. It partially prevents cardiovascular reflexes.
Its effects appear to be irreversible.
Pharmacokinetics:
The drug is absorbed poorly from the G.I. Tract. It has slow onset of action and long duration of action.
Therapeutic uses:
1. In combination with thiazide diuretics it is used to treat mild to moderate hypertension and is mostly used in condition when no other anti-hypertensive agent showing affect.
2. Insomnia
3. It was used to treat snakebites
4. Insanity
Adverse effects:
Drowsiness, Sedation, lassitude, depression, bradycardia, diarrhea, Gastric acid secretion, Nasal congestion, Nausea, vomiting
Contraindications:
• Peptic ulcer
• Parkinsonism
• Pheochromocytoma
Precautions:
It must be used with caution in patients of depression as it may aggravate this condition.
Mechanism of action:
Reserpine works to prevent neuronal and chromaffin granule transporters by Mg2+/ATP dependent transport mechanism.
As a consequence accumulation of catecholamine transmitters by adrenergic transmitter vesicles is prevented resulting in great depletion of transmitters in both central and peripheral neurons that can remain for days to weeks. Monoamine oxidase has the ability of degrading norepinephrine in the cytoplasm.
Actions:
1. It causes sedation due to depletion of biogenic amines centrally.
2. It decreases cardiac rate, cardiac output and blood pressure.
3. It may also decrease peripheral vascular resistance.
4. It partially prevents cardiovascular reflexes.
Its effects appear to be irreversible.
Pharmacokinetics:
The drug is absorbed poorly from the G.I. Tract. It has slow onset of action and long duration of action.
Therapeutic uses:
1. In combination with thiazide diuretics it is used to treat mild to moderate hypertension and is mostly used in condition when no other anti-hypertensive agent showing affect.
2. Insomnia
3. It was used to treat snakebites
4. Insanity
Adverse effects:
Drowsiness, Sedation, lassitude, depression, bradycardia, diarrhea, Gastric acid secretion, Nasal congestion, Nausea, vomiting
Contraindications:
• Peptic ulcer
• Parkinsonism
• Pheochromocytoma
Precautions:
It must be used with caution in patients of depression as it may aggravate this condition.
Reserpine
It is a plant alkaloid derived from the roots of plant Rauwolfia Serpentina.
Mechanism of action:
Reserpine works to prevent neuronal and chromaffin granule transporters by Mg2+/ATP dependent transport mechanism.
As a consequence accumulation of catecholamine transmitters by adrenergic transmitter vesicles is prevented resulting in great depletion of transmitters in both central and peripheral neurons that can remain for days to weeks. Monoamine oxidase has the ability of degrading norepinephrine in the cytoplasm.
Mechanism of action:
Reserpine works to prevent neuronal and chromaffin granule transporters by Mg2+/ATP dependent transport mechanism.
As a consequence accumulation of catecholamine transmitters by adrenergic transmitter vesicles is prevented resulting in great depletion of transmitters in both central and peripheral neurons that can remain for days to weeks. Monoamine oxidase has the ability of degrading norepinephrine in the cytoplasm.
Adrenergic neuron blocking drugs
These drugs decrease the delivery of catecholamines such as norepinephrine to adrenergic receptors.
Norepinephrine:
It is an adrenergic neurotransmitter. It is stored in the granular organelles. It is secreted by adrenal glands.
Synthesis:
It is produced in sympathetic adrenergic neurons and attaches to adrenergic receptors.
1. It elevates blood pressure and breathing rate.
2. It elevates blood sugar.
3. It causes a decline in the activity of the intestines.
Norepinephrine:
It is an adrenergic neurotransmitter. It is stored in the granular organelles. It is secreted by adrenal glands.
Synthesis:
It is produced in sympathetic adrenergic neurons and attaches to adrenergic receptors.
Actions:
1. It elevates blood pressure and breathing rate.
2. It elevates blood sugar.
3. It causes a decline in the activity of the intestines.
Classification of Anti-hypertensive drugs
1. Adrenergic neuron blocking drugs:
Bethanidine, Methoserpidine, Reserpine, Syrosingopine, Guanthedine
2. Antihypertensive direct vasodilators:
Diazoxide, Dihydralazine, Hydralazine, Minoxidil, Sodium nitroprusside
3. Centrally acting sympatholytic antihypertensive drugs:
Clonidine, Guanabenz, Guanfacine, Labetol, α-methyldopa
4. Ca2+ channel blockers:
a. Diphenylalkylamines:
Verapamil
b. Benzothiazepines:
Diltiazem
c. Dihydropyridines:
Amlodipine, Felodipine, Isradipine, Nicardipine, Nifedipine, Nisoldipine, Nitrendipine
5. Diuretics:
Bumetanide, Furosemide, Hydrochlorthiazide, Methyclothiazide, Polythiazide, Quinthazone, Spironolactone, Triamterene, Trichlomethiazide
6. Drugs acting on Renin angiotensin system:
a. ACE inhibitors:
Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril, Trandolapril
b. Angiotensin II receptor antagonist:
Candesartan cilexetil, Losartan, Saralasin, Valsartan
7. Drugs acting on Serotonin receptors:
Ketanserin, Urapidil
8. Ganglionic blocking agents:
Mecamylamine hydrochloride, Pentamethonium bromide, Pentolinium, Trimethaphan camsylate
9. Monoamine oxidase inhibitor:
Pargyline hydrochloride
10. Peripheral anti-adrenergic drugs:
a. α-blockers:
Phenoxybenzamine, Phentolamine,
b. α1-blockers:
Doxazosin, Prazosin, Terazosin
c. β-blockers:
Atenolol, Metoprolol, Nadolol, Propranolol, Timolol
d. α and β blockers:
Labetalol
11. Plant products:
Cryptenamine acetates, Reserpine, Veratridine
12. Miscellaneous:
Bretylium
Bethanidine, Methoserpidine, Reserpine, Syrosingopine, Guanthedine
2. Antihypertensive direct vasodilators:
Diazoxide, Dihydralazine, Hydralazine, Minoxidil, Sodium nitroprusside
3. Centrally acting sympatholytic antihypertensive drugs:
Clonidine, Guanabenz, Guanfacine, Labetol, α-methyldopa
4. Ca2+ channel blockers:
a. Diphenylalkylamines:
Verapamil
b. Benzothiazepines:
Diltiazem
c. Dihydropyridines:
Amlodipine, Felodipine, Isradipine, Nicardipine, Nifedipine, Nisoldipine, Nitrendipine
5. Diuretics:
Bumetanide, Furosemide, Hydrochlorthiazide, Methyclothiazide, Polythiazide, Quinthazone, Spironolactone, Triamterene, Trichlomethiazide
6. Drugs acting on Renin angiotensin system:
a. ACE inhibitors:
Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril, Trandolapril
b. Angiotensin II receptor antagonist:
Candesartan cilexetil, Losartan, Saralasin, Valsartan
7. Drugs acting on Serotonin receptors:
Ketanserin, Urapidil
8. Ganglionic blocking agents:
Mecamylamine hydrochloride, Pentamethonium bromide, Pentolinium, Trimethaphan camsylate
9. Monoamine oxidase inhibitor:
Pargyline hydrochloride
10. Peripheral anti-adrenergic drugs:
a. α-blockers:
Phenoxybenzamine, Phentolamine,
b. α1-blockers:
Doxazosin, Prazosin, Terazosin
c. β-blockers:
Atenolol, Metoprolol, Nadolol, Propranolol, Timolol
d. α and β blockers:
Labetalol
11. Plant products:
Cryptenamine acetates, Reserpine, Veratridine
12. Miscellaneous:
Bretylium
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