CALCIUM CHANNEL BLOCKERS
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1 CALCIUM CHANNEL BLOCKERS Calcium channel blockers (CCB) prevent calcium from entering cells (mainly of the heart and blood vessel walls). Calcium channel blockers, also called calcium antagonists, are used to treat various conditions, including high blood pressure, angina, Raynaud's phenomenon and some arrhythmias. They are also used to try to stop premature labour in pregnancy. DIHYDROPYRIDINES of I (nifedipine) and II (amlodipine) generation BENZOTHIAZEPINE (diltiazem) PHENYLALKYLAMINES (verapamil) PIPERAZINE (flunarizine) NIFEDIPINE VERAPAMIL DILTIAZEM AMLODIPINE
2 Voltage-operated Ca ++ CHANNELS (VOCCs) TYPE VOLTAGE MOST OFTEN FOUND IN L-TYPE CALCIUM CHANNEL ("LONG-LASTING" AKA "DHP RECEPTOR") HVA (high voltage activated) Skeletal muscle, smooth muscle, bone (osteoblasts), ventricular myocytes (responsible for prolonged action potential in cardiac cell; also termed DHP receptors), dendrites and dendritic spines of cortical neurones L-Type channel blockers are used as antihypertensive and antiarrhythmic drugs P-TYPE CALCIUM CHANNEL ("PURKINJE") /Q-TYPE CALCIUM CHANNEL N-TYPE CALCIUM CHANNEL ("NEURAL"/"NON-L") R-TYPE CALCIUM CHANNEL ("RESIDUAL") T-TYPE CALCIUM CHANNEL ("TRANSIENT") HVA (high voltage activated) HVA (high-voltageactivated) intermediatevoltageactivated low-voltageactivated Purkinje neurons in the cerebellum / Cerebellar granule cells Throughout the brain and peripheral nervous system. Cerebellar granule cells, other neurons neurons, cells that have pacemaker activity, bone (osteocytes) T-Type channel blockers are used as antiepileptic and neuropathic painkiller drugs
3 L-TYPE CALCIUM CHANNEL 1 SUBUNIT DIHYDROPYRIDINE PHENYLALKYLAMINE BENZOTHIAZEPINE PHENYLALKYILAMINE bind to intracellular IV6 segment. DIHYDROPYRIDINE bind to extracellular site on III5-III6 loop BENZOTHIAZEPINE bind in between III and IV transmembrane segment
4 CALCIUM CHANNEL BLOCKERS DIHYDROPYRIDINES bind on extracellular portion DIHYDROPYRIDINES CAN BIND AT CHANNEL RESTING STATE LIPOPHILICITY IMPLICATIONS PHENYLALKYLAMINES and BENZOTHIAZEPINES Bind on intracellular site PHENYLALKYLAMINES AND BENZOTHIAZEPINES BIND preferentially after channel activation (opening) DURING INACTIVE STATE. Therefore their binding is USE-DEPENDENT VASCULAR EFFECT PREVALENT ACTIVITY ON PRECAPILLARY RESISTANCE ARTERIES CARDIAC EFFECT ON CONDUCTANCE FIBERS
5 CALCIUM CHANNEL BLOCKERS - NOMENCLATURE amlodipine (NORVASC, ANTACAL, MONOPINA) 5mg & 10mg felodipine (FELODAY, PLENDIL, PREVEX) 5mg & 10mg barnidipine (LIBRADIN, OSIPINE, VASEXTEN) 10mg & 20mg isradipine (LOMIR SRO, CLIVOTEN, ESRADIN) 5mg lacidipine (LACIPIL, LACIREX) 4mg & 6mg lercanidipine (ZANEDIP, LERCADIP, CARDIOVASC) 10mg & 20mg manidipine (IPERTEN, VASCOMAN) 20mg nicardipine (NICARDAL, NIMICOR, PERDIPINA, ecc.) 20mg & 40mg nifedipine (ADALAT, NIFEDICOR, generico) 20mg, 30mg, 60mg «CRONO» nisoldipine (SYSCOR) 10mg nitrendipine (BAYPRESS, DEITEN) 20mg dilthiazem (TILDIEM, generic) verapamil (ISOPTIN, generic) gallopamil (PROCORUM, ALGOCOR) 50mg & 100mg
6 MAIN PK FEATURES OF CCBs DOSE NIFEDIPINE VERAPAMIL Oral Intravenous Plasma concentrations Protein binding Liver metabolism 1 passage Half-life (t 1/2 ) mg 8 h mg kg ng ml % 3-5 h mg 8 h mg kg ng ml % 5-10 h
7 MEDICAL USE FOR CCBs DHP - SELECTIVE VASODILATORS NON- DHP: EQUIPOTENT FOR CARDIAC TISSUE AND VASCULATURE
8 MEDICAL USE FOR CCBs HYPERTENSION By causing vascular smooth muscle relaxation, CCBs (DHP) decrease systemic vascular resistance, which lowers arterial blood pressure. These drugs primarily affect arterial resistance vessels, with only minimal effects on venous capacitance vessels. Reducing peripheral vascular resistance, however, is accompanied by compensatory mechanism increasing heart rate, inotropic stimulation, and renin release. These common effects of DHP, especially at the beginning of treatment, tend to reduce during the first two weeks for baroreceptor adjustments
9 MEDICAL USE FOR CCBs ANGINA The anti-anginal effects of CCBs are derived from their vasodilator and cardiodepressant actions. Systemic vasodilation reduces arterial pressure, which reduces ventricular afterload (wall stress) thereby decreasing oxygen demand. The more cardioselective CCBs (verapamil and diltiazem) decrease heart rate and contractility, which leads to a reduction in myocardial oxygen demand, which makes them excellent antianginal drugs. CCBs can also dilate coronary arteries and prevent or reverse coronary vasospasm (as occurs in Printzmetal's variant angina), thereby increasing oxygen supply to the myocardium.
10 MEDICAL USE FOR CCBs ARRHYTHMIA The antiarrhythmic properties (Class IV antiarrhythmics) of CCBs are related to their ability to decrease the firing rate of aberrant pacemaker sites within the heart, but more importantly are related to their ability to decrease conduction velocity and prolong repolarization, especially at the atrioventricular node. This latter action at the atrioventricular node helps to block reentry mechanisms, which can cause supraventricular tachycardia.
11 MEDICAL USE FOR CCBs CEREBRAL VASOSPASM Some CCBs may be used to treat migraine headaches or vertigo. They may also prevent cerebral ischemic damage from reactive vasospasm after subarachnoid hemorrhage by dilating cerebral vessels and increasing blood flow.
12 MOST COMMON SIDE EFFECTS OF CCBS DIHYDROPIRYDINE - Nifedipine (18%) Distal edema Headache Vertigo Fatigue, dizziness Postural hypotension/ reflex tachycardia Palpitation Aggravamento dell angina PHENYLALKYLAMINE - Verapamil (10%) Constipation AV Block, bradicardia Insufficienza cardiaca Vertigo, headache, dizziness BENZOTHIAZEPINE - Diltiazem (5%) AV Block, bradycardia Vertigo, dizziness Rashes Headache
13 ATP-sensitive K + -channels OPENERS These drugs hyperpolarize the smooth muscle, which closes voltage-gated calcium channels and decreases intracellular calcium. With less calcium available to combine with calmodulin, there is less activation of myosin light chain kinase and phosphorylation of myosin light chains. This leads to relaxation and vasodilation. Because small arteries and arterioles normally have a high degree of smooth muscle tone, these drugs are particular effective in dilating these resistance vessels, decreasing systemic vascular resistance, and lowering arterial pressure. The fall in arterial pressure leads to reflex cardiac stimulation (baroreceptor-mediated tachycardia). DIAZOXIDE MINOXIDIL
14 ATP-sensitive K + -channels These channels are directly linked to the metabolic cell state. Channel is CLOSED when intracellular ATP concentration is HIGH (100 µm). Channel is OPEN when intracellular ATP concentration is LOW (less than 100 µm). PANCREAS: When glycemia is high, glucose enters the cell by GluT2, ATP increases and the K-channel closes. K-channel closing depolarizes the cell, allowing opening of Calcium-channels and subsequent release of insulin from intracellular vescicles. NEURONs: K-channels control depolarization frequency, reducing it when intracellular energy is low. CV SYSTEM: K-channel opening results in cell hyperpolarization, therefore inhibiting Cachannel opening and subsequent cell activation.
15 DIAZOXIDE EMERGENCY TREATMENT on HYPERTENSION (no pheocromocytoma) EV ADMINISTRATION Fast-induced effect Binds plasma proteins (90%), Liver metabolism, renal excretion EMERGENCY TREATMENT on HYPOGLYCEMIC STATE (insulinoma) ORAL ADMINISTRATION (PROGLICEM ) 25 o 100 mg. Bioavailability > 80% Variable half-life (20 40 h)
16 MINOXIDIL Common side effects to minoxidil include headaches, flushing and reflex tachycardia. The potent vasodilator actions of minoxidil can lead to fluid retention and edema formation. Reflex cardiac stimulation can precipitate angina in patients with coronary artery disease. Minoxidil produces T wave changes in a high percentage (~60%) of patients under chronic treatment. One of the most noted side effects of minoxidil is hypertrichosis, a thickening and enhanced pigmentation of body hair, and therefore this drug is more commonly used for treating baldness.
17 ENDOTHELIN-1 RECEPTOR ANTAGONISTS Endothelin-1 (ET-1) is produced mainly by vascular endothelial cells and exerts both vasoconstriction and vascular smooth muscle cells proliferation. ET-1 biological activity depends on activation of ETA and ETB receptor subtypes. ETA receptors are prevalently expressed on vascular smooth muscle cells, and are particularly important on pulmunar arteries. ETB receptors sare ubiquitously expressed on endothelial cells and their activation results in increased release of NO and prostacyclin (with subsequent vasodilatant effects). Their role on pulmunary arteries includes also clearing of circulating ET-1.
18 ENDOTHELIN-1 EFFECTS, RECEPTORS and ANTAGONISTS
19 BOSENTAN ENDOTHELIN-1 RECEPTOR BLOCKERS Bosentan is a competitive antagonist of ET-A and ET-B receptors, with a slightly higher affinity for ET-A than ET-B. Bosentan is indicated mainly for the treatment of pulmonary hypertension. In Europe, bosentan is also approved for reducing the number of new digital ulcers in patients with systemic sclerosis. Due to potential hepatotoxicity and onset of anemia, bosentan requires a monthly monitoring of liver function and hematocrit. Due to a pharmacokinetic interaction, hormone-based contraception is not possible in women taking bosentan, therefore other highly reliable forms of contraception should be used instead. Bosentan is contraindicated in pregnancy because of its teratogenicity SITAXENTAN, AMBRISENTAN, ATRASENTAN are selective ET A receptor antagonists with similar medical use and comparable side effects (including teratogenicity)
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