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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)
What functional groups are present in Amlodipine?
Amlodipine contains an amino group (-NH2), a dihydropyridine ring, and a methyl ester group.
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 dihydropyridine calcium channel blocker is a type of medication that works by blocking calcium channels in blood vessels and the heart. This leads to relaxation of blood vessels, reduced heart workload, and decreased blood pressure. Examples include amlodipine and nifedipine.
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.
What are the functional groups of nifedipine?
amine group ester nitro group
What are the physicochemical characteristics of felodipine?
Felodipine is a dihydropyridine calcium channel blocker used to treat hypertension. It is a yellow crystalline powder, sparingly soluble in water, with a molecular weight of 384.5 g/mol. It has a pKa of 10. Strictly avoid grapefruit juice when taking felodipine as it can increase its levels in the blood, leading to potential side effects.
What structure lets calcium ions enter cardiac muscle cells?
The structure that allows calcium ions to enter cardiac muscle cells is the voltage-gated L-type calcium channels, also known as dihydropyridine receptors. These channels open in response to depolarization of the cell membrane, allowing calcium to flow into the cell and trigger muscle contraction.
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.
