What is dihydropyridine?

What is a Non-dihydropyridine calcium channel blockers?

Diltiazem and verapamilBoth act centrally at heart muscle contraction

What is the name of th receptors found in the membranes of the T tubules that function as voltage sensors?

dihydropyridine receptors (DHP receptors)

Drug of choice for treatment of Ventricular arrythmias associated with acute myocardial infaction tachycardia?

Digoxin, ACE inhibitors, Diuretics, CCBs(only dihydropyridine)..

What is a dihydropyridine calcium channel blocker?

A medication used to treat various heart conditions such as high blood pressurs, atrial fibrullation, atrial flutter and tachycardia among others

What is the therapeutic name of drug STAMLO?

STAMLO is the international name for amlodipine. It is better known in the US as Norvasc. It is a dihydropyridine calcium channel blocker used to lower blood pressure.

How does nifedipine treat cardiac ischemia?

Cardiac ischemia occurs when there is reduced blood flow to the coronary arteries This usually occurs due to the formation of a plaque in the coronary artery resulting in the interior of the artery become narrowing and hence reduced blood flow to the heart. The blood contains oxygen so the heart receives less oxygen. Angina or chest pain will occur as a symptom of myocardial ischemia. Coronary blood flow is determined by the heart's oxygen demand. Nitric oxide can be released from healthy endothelium cells to result in vasodilation and increased blood flow. However, endothelium cells which are damaged by plagues will release fewer nitric oxide. The presence of plagues in blood vessels hence results in less vasodilation in its area. Nifedipine is a dihydropyridine. It can treat cardiac ischemia by acting as a vasodilator through the inhibition L-type voltage-sensitive calcium channels of smooth muscles. More blood will hence flow to the heart and meet its oxygen demands. It doesn't slow down cardiac conduction so it has no anti-arrthymic action. Although nifedipine has a negative inotropic effect, it is overshadowed by a reflex increase in heart rate and decreased afterload so it can ultimately improve blood flow to the heart.

What are the long term effects of the drug calcium channel blocker?

Most people who take calcium-channel blockers have no side-effects, or only minor ones. Because of their action to relax and widen arteries, some people develop flushing and headache. These tend to ease over a few days if you continue to take the tablets. Mild ankle swelling is also quite common, particularly with dihydropyridine calcium-channel blockers. Constipation is quite a common side-effect, especially with verapamil. You can often deal with this by increasing the amount of fibre that you eat, and increasing the amount of water and other fluids that you drink. Other side-effects are uncommon and include: feeling sick, palpitations, tiredness, dizziness, and rashes. This is not a complete list of all possible known side-effects. Read the information leaflet that comes with your particular brand for a full list of possible side-effects, but be optimistic: don't necessarily be put off taking these tablets. Serious side-effects are rare, and it's wise not to stop calcium-channel blockers without speaking to your doctor.

What is most directly responsible for the coupling of excitation to contraction of skeletal muscle fibers?

Skeletal muscleIn skeletal muscle the method of excitation contraction coupling relies on the ryanodine receptor being activated by a domain spanning the space between the T tubules and the sarcoplasmic reticulum to produce the calcium transient responsible for allowing contraction. The alpha motor neuron produces an action potential that propagates down its axon to the neuromuscular junction.The action potential is sensed by a voltage-dependent calcium channel which causes an influx of Ca2+ ions which causes exocytosis of synaptic vesicles containing acetylcholine.Acetylcholine diffuses across the synapse and binds to nicotinic acetylcholine receptors on the myocyte, which causes an influx of Na+ and an efflux of K+ and generation of an end-plate potential.The end-plate potential propagates throughout the myocyte's sarcolemma and into the T-tubule system.The T-tubule contains dihydropyridine receptors which are voltage-dependent calcium channels and are activated by the action potential.The dihydropyridine receptors transmit the voltage-mediated signal through a mechanical linkage to the ryanodine receptors in the sarcoplasmic reticulum.Ryanodine receptors undergo a conformational change that opens their channel.Opening of the Ryanodine receptors causes and flow of Ca2+ from the sarcoplasmic reticulum into the cytoplasm. In this release, Ca2+ unbinds from the calcium-binding protein called calsequestrin.Ca2+ released from the sarcoplasmic reticulum binds to Troponin C on actin filaments, which subsequently leads to the troponin complex being physically moved aside to uncover cross-bridge binding sites on the actin filament.By hydrolyzing ATP, myosin forms a cross bridges with the actin filaments, and pulls the actin toward the center of the sarcomere resulting in contraction of the sarcomere.Activation of the cross-bridge cycling may induce a shortening of the sarcomeres and the muscle as a whole, but not if the tension is insufficient to overcome the load imparted on the muscle.Simultaneously, the sarco/endoplasmic reticulum Ca2+-ATPase actively pumps Ca2+ back into the sarcoplasmic reticulum where Ca2+ rebinds to calsequestrin.With Ca2+ no longer bound to troponin C, the troponin complex slips back to its blocking position over the binding sites on actin.Since cross-bridge cycling is ceasing then the load on the muscle causes the inactive sarcomeres to lengthen.Cardiac muscleIn cardiac muscle, the method is dependent on a phenomenon called calcium-induced calcium release, which involves the conduction of calcium ions into the cell triggering further release of ions into the cytoplasm (about 75% of calcium present in the cytoplasm during contraction is release from the sarcoplasmic reticulum).An action potential is induced by pacemaker cells in the Sinoatrial node or Atrioventricular node and conducted from non-contractile cardiac myocytes to contractile cells through gap junctions.The action potential triggers L-type calcium channels during the plateau phase of the cardiac action potential, causing a net flux of calcium ions into the cardiac myocyte.The increase in intracellular calcium ions is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which transport calcium out into the cytosol in a positive feedback physiological response.The cytoplasmic calcium binds to Troponin C, moving the troponin complex off the actin binding site allowing the myosin head to bind to the actin filament.Using ATP hydrolysis the myosin head pulls the actin filament to the centre of the sarcomere.Intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase pump into the sarcoplasm, or ejected from the cell by the sodium-calcium exchanger or the plasma membrane calcium ATPase.Intracellular calcium concentration drops and troponin complex returns over the active site of the actin filament, ending contraction.

Why can't a cardiac muscle be completely tetanized?

Cardiac muscle doesn't go into tetanic contraction due to the effect of calcium ions which are slowly released into the cell during an action potential, prolonging the action potential. As a result, the graph for electrical activity in cardiac cells has a 'plateau' area because of the release of calcium and the decreased membrane permeability to potassium. By the time the action potential is over, the refractory period (channel inactivation period) for the ions are over, and the cardiac cell is relaxed and ready to be excited again. skeletal action potential = 5-10 msec. cardiac action potential = 250 msec.

Should you avoid drinking grapefruit juice while taking azithromycin?

Grapefruit has a lot of Vitamin C plus some enzymes that seem to speed up things . (For a while back in the 60's- grapefruit was thought to be a fat burner. ) Some antibiotics i.e. Erythromycin and other drugs which are in this class (the Not Pencillins) do not mix well at all, especially with Garpefruit. So those of you who take Erythromycin because of your pencillin allergies should be careful; especially when taking megadoses of Vitamin C or eating grapefruit. The end result is your liver gets a big buildup of drugs it cannot handle - you are actually poisoning your self because the drugs are not working properly. Here is the science: Erythromycin competes - It does the exact same thing as Vitamin C: it inhibits the cytochrome P450 system, particularly the CYP3A4 isozyme, which can cause it to affect the metabolism of many different drugs, not just Vitamin C. I am not the pharmacist- just a smart nutritionist student who knows biochemistry. When I graduate I will sign this. In the meantime you are provided with the following quoted directly from a professional source D.McAuley, with references GlobalRPH.com His site is a great study guide as well. Just always give him credit because he has copyrighted the site. " Grapefruit juice is a potent inhibitor of the intestinal cytochrome P-450 3A4 system (specifically: CYP3A4 - mediated drug metabolism) which is responsible for the first-pass metabolism of many medications. This interaction can lead to increases in bioavailability and corresponding increases in serum drug levels. In many cases, the increased serum drug levels can produce some readily observable symptoms. Here are a few examples of adverse effects that are possible when the following medications are taken concurrently with grapefruit. (1) Excessive sedation: benzodiazepines. (2) Increased risk of rhabdomyolyis: HMG-CoA reductase inhibitors (statins)-- there are some exceptions. (3) Symptomatic hypotension: dihydropyridine calcium antagonists (some exceptions exist). (4) QT interval prolongation: astemizole, cisapride, pimozide, terfenadine. "Drug interactions may be most apparent when patients are stabilized on the affected drug and the CYP3A4 inhibitor is then added to the regimen." 5 CONVERSELY THE VITAMIN C THAT IS FACILITATED BY THE ENZYMES IN GRAPEFRUIT IS NOT ALL BAD>>>> the problem is that the drugs you take work on the same enzyme activation sites or pathways and only one thing can work well at a time or in the case of some drugs like the heart medicines the heartbeat is sped up or slowed down which is NOT what the doctor ordered when he put you on the medication. There may be some pharmacological advantages to this interaction. If the interaction is taken into account during the initialization of drug therapy it is possible to decrease drug dosages. This concept can be applied to cyclosporine therapy. If a patient regularly consumes grapefruit, lower dosages of cyclosporine will be required, which will lead to lower drug costs. IN CONCLUSION Grapefruit juice is not the only inhibitor of this enzyme system. Other drugs which have a similar effect include: clarithromycin (Biaxin ®), erythromycin (E-Mycin ®, others), itraconazole (Sporonox ®), ketoconazole (Nizoril ®), nefazodone (Serzone ®), and ritonavir (Norvir ®). " References: 1. Bailey DG, Dresser GK. Grapefruit juice-lovastatin interaction. Clin Pharmacol Ther. 2000 Jun;67(6):6902. Bistrup C, Nielsen FT, Jeppesen UE, Dieperink H. Effect of grapefruit juice on Sandimmun Neoral absorption among stable renal allograft recipients. Nephrol Dial Transplant. 2001 Feb;16(2):373-7.3. Bramer SL, Brisson J, Corey AE. Effect of multiple cilostazol doses on single dose lovastatin pharmacokinetics in healthy volunteers. Clin Pharmacokinet. 1999;37 Suppl 2:69-77.4.Damkier P, Hansen LL, Brosen K. Effect of diclofenac, disulfiram, itraconazole, grapefruit juice and erythromycin on the pharmacokinetics of quinidine. Br J Clin Pharmacol. 1999 Dec;48(6):829-38.5. Dresser GK, Spence JD, Bailey DG. Pharmacokinetic-pharmacodynamic consequences and clinical relevance of cytochrome P450 3A4 inhibition. Clin Pharmacokinet. 2000 Jan;38(1):41-57.6. Dresser GK, Bailey DG, Carruthers SG. Grapefruit juice--felodipine interaction in the elderly. Clin Pharmacol Ther. 2000 Jul;68(1):28-34.7.Eagling VA, Profit L, Back DJ. Inhibition of the CYP3A4-mediated metabolism and P-glycoprotein-mediated transport of the HIV-1 protease inhibitor saquinavir by grapefruit juice components. Br J Clin Pharmacol. 1999 Oct;48(4):543-52.8. Evans AM. Influence of dietary components on the gastrointestinal metabolism and transport of drugs Ther Drug Monit. 2000 Feb;22(1):131-6.9. Fukuda K, Guo L, Ohashi N, Yoshikawa M, Yamazoe Y. Amounts and variation in grapefruit juice of the main components causing grapefruit-drug interaction. J Chromatogr B Biomed Sci Appl. 2000 May 12;741(2):195-203.10. Fuhr U. [Clinically significant" new drug interactions]. Med Klin. 2000 May;95(1 Spec No):18-22.11. Fuhr U, Maier-Bruggemann A, Blume H, Muck W, Unger S, Kuhlmann J, Huschka C, Zaigler M, Rietbrock S, Staib AH. Grapefruit juice increases oral nimodipine bioavailability. Int J Clin Pharmacol Ther. 1998 Mar;36(3):126-32.12. Garg SK, Kumar N, Bhargava VK, Prabhakar SK. Effect of grapefruit juice on carbamazepine bioavailability in patients with epilepsy. Clin Pharmacol Ther. 1998 Sep;64(3):286-8.13.Kanazawa S, Ohkubo T, Sugawara K. The effects of grapefruit juice on the pharmacokinetics of erythromycin. Eur J Clin Pharmacol. 2001 Jan-Feb;56(11):799-803.14. Kane GC, Lipsky JJ. Drug-grapefruit juice interactions. Mayo Clin Proc. 2000 Sep;75(9):933-42.15. Lee AJ, Chan WK, Harralson AF, Buffum J, Bui BC. The effects of grapefruit juice on sertraline metabolism: an in vitro and in vivo study. Clin Ther. 1999 Nov;21(11):1890-9.16.Lilja JJ, Kivisto KT, Neuvonen PJ. Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin. Clin Pharmacol Ther. 1999 Aug;66(2):118-27.17.Lilja JJ, Kivisto KT, Backman JT, Lamberg TS, Neuvonen PJ. Grapefruit juice substantially increases plasma concentrations of buspirone. Clin Pharmacol Ther. 1998 Dec;64(6):655-60.18. Lilja JJ, Kivisto KT, Neuvonen PJ. Duration of effect of grapefruit juice on the pharmacokinetics of the CYP3A4 substrate simvastatin. Clin Pharmacol Ther. 2000 Oct;68(4):384-90.19. Lilja JJ, Kivisto KT, Backman JT, Neuvonen PJ. Effect of grapefruit juice dose on grapefruit juice-triazolam interaction: repeated consumption prolongs triazolam half-life. Eur J Clin Pharmacol. 2000 Aug;56(5):411-5.20. Libersa CC, Brique SA, Motte KB, Caron JF, Guedon-Moreau LM, Humbert L, Vincent A, Devos P, Lhermitte MA. Dramatic inhibition of amiodarone metabolism induced by grapefruit juice. Br J Clin Pharmacol. 2000 Apr;49(4):373-8.21. Mitsunaga Y, Takanaga H, Matsuo H, Naito M, Tsuruo T, Ohtani H, Sawada Y. Effect of bioflavonoids on vincristine transport across blood-brain barrier. Eur J Pharmacol. 2000 May 3;395(3):193-201.22. Ozdemir M, Aktan Y, Boydag BS, Cingi MI, Musmul A. Interaction between grapefruit juice and diazepam in humans. Eur J Drug Metab Pharmacokinet. 1998 Jan-Mar;23(1):55-9.23. Singh BN. Effects of food on clinical pharmacokinetics. Clin Pharmacokinet. 1999 Sep;37(3):213-55. Review.24. Zhang H, Wong CW, Coville PF, Wanwimolruk S. Effect of the grapefruit flavonoid naringin on pharmacokinetics of quinine in rats. Drug Metabol Drug Interact. 2000;17(1-4):351-63. © D.McAuley, GlobalRPH.com 2001

What is dihydropyridine?

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