They cause blockade ganglion receptors by occupying sites in or on the ion channels that are regulated by nicotinic cholinergic receptors. They do not occupy cholinergic receptor itself.
Sunday, April 10, 2011
Competitive ganglion blockers
Mechanism of action:
They cause non-depolarizing competitive blockage of ganglia. They compete with acetylcholine at postsynaptic nicotinic receptors.
Actions:
Since the ganglia of sympathetic as well as parasympathetic nervous system are cholinergic so these agents obstruct the outflow through these systems.
Blockade of sympathetic outflow causes a decrease in firmness of the arterioles resulting in the reduced peripheral vascular resistance leading to postural or orthostatic hypotension.
Blockade of parasympathetic outflow causes:
1. A prominent reduction in the motility of the GI tract.
2. Dry mouth
3. Cycloplegia with a decrease in accommodation.
4. Precipitation of urinary retention in men with prostatic hypertrophy.
Adverse effects:
Mostly autonomic effects
They cause non-depolarizing competitive blockage of ganglia. They compete with acetylcholine at postsynaptic nicotinic receptors.
Actions:
Since the ganglia of sympathetic as well as parasympathetic nervous system are cholinergic so these agents obstruct the outflow through these systems.
Blockade of sympathetic outflow causes a decrease in firmness of the arterioles resulting in the reduced peripheral vascular resistance leading to postural or orthostatic hypotension.
Blockade of parasympathetic outflow causes:
1. A prominent reduction in the motility of the GI tract.
2. Dry mouth
3. Cycloplegia with a decrease in accommodation.
4. Precipitation of urinary retention in men with prostatic hypertrophy.
Adverse effects:
Mostly autonomic effects
Clonidine
Mechanism of action:
It causes activation of α2 receptors in the vasomotor center of brain that causes a decrease in sympathetic outflow to the peripheral vascular bed.
Actions:
Its intravascular injection causes a direct activation of peripheral α-adrenergic receptors resulting in a short time elevated systolic and diastolic pressure. After this, there is a reduction of cardiac output and cardiac rate resulting in the fall of blood pressure.
It causes a decrease in plasma renin activity.
It causes an elevated vagal discharge along with promoted baroreceptor reflex sensitivity.
It causes a reduction of renal vascular resistance but does not affect renal blood flow.
It causes sodium and water retention and that is why they are taken along with diuretics.
Pharmacokinetics:
It is well absorbed orally and is excreted by the kidney.
Therapeutic uses:
It is used for hypertensive patients especially in patients of renal impairment.
Adverse effects:
Sedation, drowsiness, drying of the nasal mucosa, fluid retention, headache and sweating,
Dosage:
It may be given in the dose of 0.2-1.2 mg/day. Its transdermal patches can give dose for up to 1 week.
It causes activation of α2 receptors in the vasomotor center of brain that causes a decrease in sympathetic outflow to the peripheral vascular bed.
Actions:
Its intravascular injection causes a direct activation of peripheral α-adrenergic receptors resulting in a short time elevated systolic and diastolic pressure. After this, there is a reduction of cardiac output and cardiac rate resulting in the fall of blood pressure.
It causes a decrease in plasma renin activity.
It causes an elevated vagal discharge along with promoted baroreceptor reflex sensitivity.
It causes a reduction of renal vascular resistance but does not affect renal blood flow.
It causes sodium and water retention and that is why they are taken along with diuretics.
Pharmacokinetics:
It is well absorbed orally and is excreted by the kidney.
Therapeutic uses:
It is used for hypertensive patients especially in patients of renal impairment.
Adverse effects:
Sedation, drowsiness, drying of the nasal mucosa, fluid retention, headache and sweating,
Dosage:
It may be given in the dose of 0.2-1.2 mg/day. Its transdermal patches can give dose for up to 1 week.
Methyldopa
Mechanism of action:
Methyldopa is changed into α-methylnorepinephrine, which replaces norepinephrine in adrenergic nerve granules. This α-methylnorepinephrine, interacts with presynaptic central α2-adrenergic receptors, on release by nerve stimulation. On interaction it causes a decrease in sympathetic outflow and total peripheral resistance resulting in reduction of arterial pressure.
Methyldopa also blocks dopa decarboxylase resulting in the reduction of the stores of norepinephrine in the sympathetic nervous system leading to a decrease in blood pressure.
Actions:
This causes a decrease in renal vascular resistance, which is probably due to weak vasoconstrictor effect of α-methylnorepinephrine in renal vessels than norepinephrine.
It does not affect the blood flow to the important organs.
Pharmacokinetics:
Its onset of action is 120 minutes and duration of action is 17-25 hours.
Therapeutic uses:
It can be used for mild to moderately serious hypertension. It is especially useful for hypertensive patients, who are pregnant or have renal insufficiency.
Adverse effects:
Sedation, lassitude, Hemolytic anemia, orthostatic hypotension, rebound hypotension on sudden withdrawal, depression
Contraindications:
It is contraindicated in
1. pheochromocytoma
2. during the administration of MAO inhibitors
3. acute hepatic disease
Dosage:
It is given orally in the dose of 1-2 gm in divided doses.
Methyldopa is changed into α-methylnorepinephrine, which replaces norepinephrine in adrenergic nerve granules. This α-methylnorepinephrine, interacts with presynaptic central α2-adrenergic receptors, on release by nerve stimulation. On interaction it causes a decrease in sympathetic outflow and total peripheral resistance resulting in reduction of arterial pressure.
Methyldopa also blocks dopa decarboxylase resulting in the reduction of the stores of norepinephrine in the sympathetic nervous system leading to a decrease in blood pressure.
This causes a decrease in renal vascular resistance, which is probably due to weak vasoconstrictor effect of α-methylnorepinephrine in renal vessels than norepinephrine.
It does not affect the blood flow to the important organs.
Pharmacokinetics:
Its onset of action is 120 minutes and duration of action is 17-25 hours.
Therapeutic uses:
It can be used for mild to moderately serious hypertension. It is especially useful for hypertensive patients, who are pregnant or have renal insufficiency.
Adverse effects:
Sedation, lassitude, Hemolytic anemia, orthostatic hypotension, rebound hypotension on sudden withdrawal, depression
Contraindications:
It is contraindicated in
1. pheochromocytoma
2. during the administration of MAO inhibitors
3. acute hepatic disease
Dosage:
It is given orally in the dose of 1-2 gm in divided doses.
Saturday, April 9, 2011
ACE inhibitors
Mechanism of action:
They block the converting enzyme peptidyl dipeptidase that hydrolyzes and causes the conversion of (decapeptide) angiotensin I to (octapeptide) angiotensin II, resulting in the decrease of vasoconstrictor effect of angiotnesin II.
It also causes an increase of bradykinin, which has a vasodilator activity.
Actions:
1. They cause a decrease in total peripheral resistance and mean arterial blood pressure and either no change or an increase in cardiac output.
2. They do not result in reflex sympathetic stimulation and can be used safely and effectively in patients with ischemic heart disease.
Therapeutic uses:
They can be used for:
1. Mild to moderate essential hypertension and renovascular hypertension
2. Chronic congestive heart failure
3. Left ventricular systolic dysfunction
4. They can also be used in diabetic proteinuria
Adverse effects:
Headaches, dizziness, acute renal failure, hyperkalemia, dry cough, wheezing, skin rashes, angioedema
Contraindications:
1. aortic constriction
2. renal disturbance
3. pregnancy and lactation
4. bilateral renal artery constriction
They block the converting enzyme peptidyl dipeptidase that hydrolyzes and causes the conversion of (decapeptide) angiotensin I to (octapeptide) angiotensin II, resulting in the decrease of vasoconstrictor effect of angiotnesin II.
Actions:
1. They cause a decrease in total peripheral resistance and mean arterial blood pressure and either no change or an increase in cardiac output.
Therapeutic uses:
They can be used for:
1. Mild to moderate essential hypertension and renovascular hypertension
2. Chronic congestive heart failure
3. Left ventricular systolic dysfunction
4. They can also be used in diabetic proteinuria
Adverse effects:
Headaches, dizziness, acute renal failure, hyperkalemia, dry cough, wheezing, skin rashes, angioedema
Contraindications:
1. aortic constriction
2. renal disturbance
3. pregnancy and lactation
4. bilateral renal artery constriction
Saralasin
It is a partial agonist. It is a peptide analogue of angiotensin II.
Mechanism of action:
It competitively inhibits of angiotensin II receptors.
Actions:
1. it blocks the vasoconstrictor and aldosterone releasing effects of angiotensin II and reduces blood pressure in increased renin states e.g. in renal artery constriction.
2. Due to its weak agonist activity it may increase Blood pressure by rapid administration to persons without increased circulating angiotensin II.
Adverse effects:
Its adverse effects are almost same to those of ACE inhibitors.
Contraindicated:
They are contraindicated in for pregnant woman.
Mechanism of action:
It competitively inhibits of angiotensin II receptors.
Actions:
1. it blocks the vasoconstrictor and aldosterone releasing effects of angiotensin II and reduces blood pressure in increased renin states e.g. in renal artery constriction.
2. Due to its weak agonist activity it may increase Blood pressure by rapid administration to persons without increased circulating angiotensin II.
Adverse effects:
Its adverse effects are almost same to those of ACE inhibitors.
Contraindicated:
They are contraindicated in for pregnant woman.
Minoxidil
Mechanism of action:
It causes dilatation of arterioles by unclosing of potassium channels. This opening of potassium channels causes hyperpolarization leading to relaxation of smooth muscles. This relaxation of smooth muscles results in the reduction of total peripheral vascular resistance. So, the blood pressure is reduced.
Actions:
Minoxidil may cause palpitations and reflex tachycardia.
It may increase the plasma renin activity caused by reflex sympathetic activity or decrease by certain unknown mechanism.
It may cause sodium and water retention.
Pharmacokinetics:
It is well absorbed orally. It is metabolized in the liver. Its duration of action is about 1-3 days.
Therapeutic uses:
1. Moderate to serious hypertension
2. severe hypertension associated with disturbance of renal function
3. topically can be used as an activator of hair growth for baldness
Adverse effects:
Headache, Tachycardia, angina, sweating, Excessive hair growth, fluid retention causing volume overload
It causes dilatation of arterioles by unclosing of potassium channels. This opening of potassium channels causes hyperpolarization leading to relaxation of smooth muscles. This relaxation of smooth muscles results in the reduction of total peripheral vascular resistance. So, the blood pressure is reduced.
Minoxidil may cause palpitations and reflex tachycardia.
It may increase the plasma renin activity caused by reflex sympathetic activity or decrease by certain unknown mechanism.
It may cause sodium and water retention.
Pharmacokinetics:
It is well absorbed orally. It is metabolized in the liver. Its duration of action is about 1-3 days.
Therapeutic uses:
1. Moderate to serious hypertension
2. severe hypertension associated with disturbance of renal function
3. topically can be used as an activator of hair growth for baldness
Adverse effects:
Headache, Tachycardia, angina, sweating, Excessive hair growth, fluid retention causing volume overload
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