These drugs are recommended when the preferred first line agents are contraindicated or ineffective.
Mainly effective in HTN having angina and diabetes.
High doses of short acting CCB should be avoided because of increase risk of MI due to excessive vasodilatation.
Diphenylalkalamine
verapamil
Benzothiazepines
Diltiazem
Dihydropyridines
Nifedipine
Amlodipine
Feldopine
Isradipine
Nicardipine
Nimodipine
MECHANISM
Force of contraction of cardiac muscles is directly related to the conc. of cystosolic calcium (free unbound).
Calcium comes from several sources.
out side the cell- where opening of voltage sensitive ca++ channels cause an immediate rise in free cystosolic ca++.
Calcium may enter by exchange of sodium ions.
Ca++ is also release from sarco plasmic reticulum and mitochondria which further increases the cystosolic level of ca++.
Ca++ ion channel are located in plasma membrane of smooth muscles and cardiac tissues.
In flux of calcium ions leads to depolarization by combining with calmoduline and activates myosin kinase phosphate which enable the myosin to interact with actin to cause muscle contraction.
CCBs binds to these channels and alter their conformation and prevents the entry of ca++
in to cells and produce smooth muscles relaxation and suppress cardiac activity.
All CCBs are arteriolar vaso dilations that decreases smooth muscles tone and vascular resistance.
Mainly effective in HTN having angina and diabetes.
High doses of short acting CCB should be avoided because of increase risk of MI due to excessive vasodilatation.
Diphenylalkalamine
verapamil
Benzothiazepines
Diltiazem
Dihydropyridines
Nifedipine
Amlodipine
Feldopine
Isradipine
Nicardipine
Nimodipine
MECHANISM
Force of contraction of cardiac muscles is directly related to the conc. of cystosolic calcium (free unbound).
Calcium comes from several sources.
out side the cell- where opening of voltage sensitive ca++ channels cause an immediate rise in free cystosolic ca++.
Calcium may enter by exchange of sodium ions.
Ca++ is also release from sarco plasmic reticulum and mitochondria which further increases the cystosolic level of ca++.
Ca++ ion channel are located in plasma membrane of smooth muscles and cardiac tissues.
In flux of calcium ions leads to depolarization by combining with calmoduline and activates myosin kinase phosphate which enable the myosin to interact with actin to cause muscle contraction.
CCBs binds to these channels and alter their conformation and prevents the entry of ca++
in to cells and produce smooth muscles relaxation and suppress cardiac activity.
All CCBs are arteriolar vaso dilations that decreases smooth muscles tone and vascular resistance.
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