Nifedipine
Calcium Channel Blockers
Diltiazem
Calcium
Dihydropyridines
Calcium Channels, L-Type
Calcium Channels
Delayed-Action Preparations
Gingival Overgrowth
Nicardipine
Calcium Channel Agonists
Tocolytic Agents
Atenolol
Muscle Contraction
omega-Conotoxin GVIA
Felodipine
Hypertension
Mibefradil
Dose-Response Relationship, Drug
Muscle, Smooth
Pyridines
Membrane Potentials
Angina Pectoris
Guinea Pigs
Tocolysis
Potassium Chloride
Gallopamil
Amlodipine
Drug Interactions
Potassium
Nitrendipine
Double-Blind Method
Norepinephrine
Nisoldipine
Cytochrome P-450 CYP3A
Ryanodine
Isradipine
Antihypertensive Agents
Neural modulation of cephalexin intestinal absorption through the di- and tripeptide brush border transporter of rat jejunum in vivo. (1/2286)
Intestinal absorption of beta-lactamine antibiotics (e.g., cefixime and cephalexin) has been shown to proceed through the dipeptide carrier system. In a previous study, nifedipine (NFP), an L-type calcium channel blocker, enhanced the absorption of cefixime in vivo but not in vitro, and it was suggested that neural mechanisms might be involved in the effect of NFP. The aim of the present study was to assess the involvement of the nervous system on the intestinal absorption of cephalexin (CFX). To investigate this, we used a single-pass jejunal perfusion technique in rats. NFP and diltiazem enhanced approximately 2-fold the plasma levels of CFX in treated rats versus untreated controls. NFP also increased approximately 2-fold the CFX level in portal plasma and increased urinary excretion of CFX, thus indicating that CFX did effectively increase CFX intestinal absorption. Perfusing high concentrations of dipeptides in the jejunal lumen competitively reduced CFX absorption and inhibited the enhancement of CFX absorption produced by NFP. Hexamethonium and lidocaine inhibited the effect of NFP, whereas atropine, capsaicin, clonidine, and isoproterenol enhanced CFX absorption by the same order of magnitude as NFP. Thus, complex neural networks can modulate the function of the intestinal di- and tripeptide transporter. Sympathetic noradrenergic fibers, intestinal sensory neurons, and nicotinic synapses are involved in the increase of CFX absorption produced by NFP. (+info)Effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline release and purinergic neuroeffector transmission in rat tail artery. (2/2286)
1. The effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline (NA) and adenosine 5'-triphosphate (ATP) release from postganglionic sympathetic nerves have been investigated in rat tail arteries in vitro. Intracellularly recorded excitatory junction potentials (e.j.ps) were used as a measure of ATP release and continuous amperometry was used to measure NA release. 2. Varying the extracellular Ca2+ concentration similarly affected the amplitudes of e.j.ps and NA-induced oxidation currents evoked by trains of ten stimuli at 1 Hz. 3. The N-type Ca2+ blocker, omega-conotoxin GVIA (omega-CTX GVIA, 0.1 microM) reduced the amplitudes of both e.j.ps (evoked by trains of ten stimuli at 1 Hz) and NA-induced oxidation currents (evoked by trains of ten stimuli at 1 Hz and 50 stimuli at 10 Hz) by about 90%. 4. The omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents evoked by trains of 50 stimuli at 10 Hz were abolished by the non-selective Ca2+ channel blocker, Cd2+ (0.1 mM), and were reduced by omega-conotoxin MVIIC (0.5 microM) and omega-agatoxin IVA (40 nM). 5. Nifedipine (10 microm) had no inhibitory effect on omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents. 6. Thus both varying Ca2+ concentration and applying Ca2+ channel blockers results in similar effects on NA and ATP release from postganglionic sympathetic nerves. These findings are consistent with the hypothesis that NA and ATP are co-released together from the sympathetic nerve terminals. (+info)The Ca2+ channel blockade changes the behavioral and biochemical effects of immobilization stress. (3/2286)
We investigated how the effects of chronic immobilization stress in rats are modified by Ca2+ channel blockade preceding restraint sessions. The application of nifedipine (5 mg/kg) shortly before each of seven daily 2 h restraint sessions prevented the development of sensitized response to amphetamine as well as the stress-induced elevation of the densities of L-type Ca2+ channel in the hippocampus and significantly reduced the elevation of the densities of [3H]nitrendipine binding sites in the cortex and D1 dopamine receptors in the limbic forebrain. Neither stress, nor nifedipine affected the density of alpha 1-adrenoceptors and D1 receptors in the cerebral cortex nor D2 dopamine receptors in the striatum. A single restraint session caused an elevation of blood corticosterone level that remained unaffected by nifedipine pretreatment, but the reduction of this response during the eighth session was significantly less expressed in nifedipine-treated rats. We conclude that L-type calcium channel blockade prevents development of several stress-induced adaptive responses. (+info)Sympathetic neuroeffector transmission in the rat anococcygeus muscle. (4/2286)
1. When intracellular recordings were made from preparations of rat anococcygeus muscle, transmural nerve stimulation evoked noradrenergic excitatory junction potentials (EJPs) made up of two distinct components. Both components were abolished by either guanethidine or alpha-adrenoceptor antagonists, indicating that they resulted from the release of transmitter from sympathetic nerves and the subsequent activation of alpha-adrenoceptors. 2. The first component was associated with a transient increase in the intracellular concentration of calcium ions ([Ca2+]i) and a contraction. Although the second component was often associated with a long lasting increase in [Ca2+]i it was not associated with a contraction unless the second component initiated an action potential. 3. The increase in [Ca2+]i associated with the first component resulted from Ca2+ release from an intracellular store and from entry of Ca2+ through voltage-dependent Ca2+ channels. The increase in [Ca2+]i associated with the second component resulted only from the entry of Ca2+ through L-type Ca2+ channels (CaL channels). The depolarization associated with the initial increase in [Ca2+]i was abolished by reducing the external concentration of chloride ions ([Cl-]o), suggesting that it involved the activation of a Cl- conductance. 4. When the relationships between changes in [Ca2+]i, membrane depolarization and contraction produced by an increasing number of sympathetic nerve stimuli were determined in control, and caffeine- and nifedipine-containing solutions, it was found that an increase in [Ca2+]i recorded in nifedipine produced a larger contraction and larger membrane depolarization than did a similar increase in [Ca2+]i recorded in either control or caffeine-containing solutions. These observations indicate that Ca2+ released from stores more readily triggers contraction and membrane depolarization than does Ca2+ entry via CaL channels. (+info)Relationship between L-type Ca2+ current and unitary sarcoplasmic reticulum Ca2+ release events in rat ventricular myocytes. (5/2286)
1. The time courses of Ca2+ current and Ca2+ spark occurrence were determined in single rat ventricular myocytes voltage clamped with patch pipettes containing 0.1 microM fluo-3. Acquisition of line-scan images on a laser scanning confocal microscope was synchronized with measurement of Cd2+-sensitive Ca2+ currents. In most cells, individual Ca2+ sparks were observed by reducing Ca2+ current density with nifedipine (0.1-8 microM). 2. Ca2+ sparks elicited by depolarizing voltage-clamp pulses had a peak [Ca2+] amplitude of 289 +/- 3 nM with a decay half-time of 20.8 +/- 0.2 ms and a full width at half-maximum of 1.40 +/- 0.03 microm (mean +/- s. e.m., n = 345), independent of the membrane potential. 3. The time between the beginning of a depolarization and the initiation of each Ca2+ spark was calculated and data were pooled to construct waiting time histograms. Exponential functions were fitted to these histograms and to the decaying phase of the Ca2+ current. This analysis showed that the time constants describing Ca2+ current and Ca2+ spark occurrence at membrane potentials between -30 mV and +30 mV were not significantly different. At +50 mV, in the absence of nifedipine, the time constant describing Ca2+ spark occurrence was significantly larger than the time constant of the Ca2+ current. 4. A simple model is developed using Poisson statistics to relate macroscopic Ca2+ current to the opening of single L-type Ca2+ channels at the dyad junction and to the time course of Ca2+ spark occurrence. The model suggests that the time courses of macroscopic Ca2+ current and Ca2+ spark occurrence should be closely related when opening of a single L-type Ca2+ channel initiates a Ca2+ spark. By comparison with the data, the model suggests that Ca2+ sparks are initiated by the opening of a single L-type Ca2+ channel at all membrane potentials encountered during an action potential. (+info)Voltage-dependent entry and generation of slow Ca2+ oscillations in glucose-stimulated pancreatic beta-cells. (6/2286)
The role of voltage-dependent Ca2+ entry for glucose generation of slow oscillations of the cytoplasmic Ca2+ concentration ([Ca2+]i) was evaluated in individual mouse pancreatic beta-cells. Like depolarization with K+, a rise of the glucose concentration resulted in an enhanced influx of Mn2+, which was inhibited by nifedipine. This antagonist of L-type Ca2+ channels also blocked the slow oscillations of [Ca2+]i induced by glucose. The slow oscillations occurred in synchrony with variations in Mn2+ influx and bursts of action currents, with the elevation of [Ca2+]i being proportional to the frequency of the action currents. A similar relationship was obtained when Ca2+ was replaced with Sr2+. Occasionally, the slow [Ca2+]i oscillations were superimposed with pronounced spikes temporarily arresting the action currents. It is concluded that the glucose-induced slow oscillations of [Ca2+]i are caused by periodic depolarization with Ca2+ influx through L-type channels. Ca2+ spiking, due to intracellular mobilization, may be important for chopping the slow oscillations of [Ca2+]i into shorter ones characterizing beta-cells situated in pancreatic islets. (+info)Contribution of L-type Ca2+ current to electrical activity in sinoatrial nodal myocytes of rabbits. (7/2286)
The role of L-type calcium current (ICa,L) in impulse generation was studied in single sinoatrial nodal myocytes of the rabbit, with the use of the amphotericin-perforated patch-clamp technique. Nifedipine, at a concentration of 5 microM, was used to block ICa,L. At this concentration, nifedipine selectively blocked ICa,L for 81% without affecting the T-type calcium current (ICa,T), the fast sodium current, the delayed rectifier current (IK), and the hyperpolarization-activated inward current. Furthermore, we did not observe the sustained inward current. The selective action of nifedipine on ICa,L enabled us to determine the activation threshold of ICa,L, which was around -60 mV. As nifedipine (5 microM) abolished spontaneous activity, we used a combined voltage- and current-clamp protocol to study the effects of ICa,L blockade on repolarization and diastolic depolarization. This protocol mimics the action potential such that the repolarization and subsequent diastolic depolarization are studied in current-clamp conditions. Nifedipine significantly decreased action potential duration at 50% repolarization and reduced diastolic depolarization rate over the entire diastole. Evidence was found that recovery from inactivation of ICa,L occurs during repolarization, which makes ICa,L available already early in diastole. We conclude that ICa,L contributes significantly to the net inward current during diastole and can modulate the entire diastolic depolarization. (+info)Delayed rectifier potassium current in undiseased human ventricular myocytes. (8/2286)
OBJECTIVE: The purpose of the study was to investigate the properties of the delayed rectifier potassium current (IK) in myocytes isolated from undiseased human left ventricles. METHODS: The whole-cell configuration of the patch-clamp technique was applied in 28 left ventricular myocytes from 13 hearts at 35 degrees C. RESULTS: An E-4031 sensitive tail current identified the rapid component of IK (IKr) in the myocytes, but there was no evidence for an E-4031 insensitive slow component of IK (IKs). When nifedipine (5 microM) was used to block the inward calcium current (ICa), IKr activation was fast (tau = 31.0 +/- 7.4 ms, at +30 mV, n = 5) and deactivation kinetics were biexponential and relatively slow (tau 1 = 600.0 +/- 53.9 ms and tau 2 = 6792.2 +/- 875.7 ms, at -40 mV, n = 7). Application of CdCl2 (250 microM) to block ICa altered the voltage dependence of the IKr considerably, slowing its activation (tau = 657.1 +/- 109.1 ms, at +30 mV, n = 5) and accelerating its deactivation (tau = 104.0 +/- 18.5 ms, at -40 mV, n = 8). CONCLUSIONS: In undiseased human ventricle at 35 degrees C IKr exists having fast activation and slow deactivation kinetics; however, there was no evidence found for an expressed IKs. IKr probably plays an important role in the frequency dependent modulation of repolarization in undiseased human ventricle, and is a target for many Class III antiarrhythmic drugs. (+info)Nifedipine is an antihypertensive and calcium channel blocker medication. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve the supply of oxygen and nutrients to the heart. Nifedipine is used to treat high blood pressure (hypertension), angina (chest pain), and certain types of heart rhythm disorders.
In medical terms, nifedipine can be defined as: "A dihydropyridine calcium channel blocker that is used in the treatment of hypertension, angina pectoris, and Raynaud's phenomenon. It works by inhibiting the influx of calcium ions into vascular smooth muscle and cardiac muscle, which results in relaxation of the vascular smooth muscle and decreased workload on the heart."
Calcium channel blockers (CCBs) are a class of medications that work by inhibiting the influx of calcium ions into cardiac and smooth muscle cells. This action leads to relaxation of the muscles, particularly in the blood vessels, resulting in decreased peripheral resistance and reduced blood pressure. Calcium channel blockers also have anti-arrhythmic effects and are used in the management of various cardiovascular conditions such as hypertension, angina, and certain types of arrhythmias.
Calcium channel blockers can be further classified into two main categories based on their chemical structure: dihydropyridines (e.g., nifedipine, amlodipine) and non-dihydropyridines (e.g., verapamil, diltiazem). Dihydropyridines are more selective for vascular smooth muscle and have a greater effect on blood pressure than heart rate or conduction. Non-dihydropyridines have a more significant impact on cardiac conduction and contractility, in addition to their vasodilatory effects.
It is important to note that calcium channel blockers may interact with other medications and should be used under the guidance of a healthcare professional. Potential side effects include dizziness, headache, constipation, and peripheral edema.
Diltiazem is a calcium channel blocker medication that is used to treat hypertension (high blood pressure), angina (chest pain), and certain heart rhythm disorders. It works by relaxing the muscles of the blood vessels, which lowers blood pressure and improves blood flow to the heart. Diltiazem may also be used to reduce the risk of heart attack in patients with coronary artery disease.
The medication is available in various forms, including immediate-release tablets, extended-release tablets, and extended-release capsules. It is usually taken orally, one to three times a day, depending on the formulation and the individual patient's needs. Diltiazem may cause side effects such as dizziness, headache, nausea, and constipation.
It is important to follow the dosage instructions provided by your healthcare provider and to inform them of any other medications you are taking, as well as any medical conditions you have, before starting diltiazem.
Verapamil is a calcium channel blocker medication that is primarily used to treat hypertension (high blood pressure), angina (chest pain), and certain types of cardiac arrhythmias (irregular heart rhyats). It works by relaxing the smooth muscle cells in the walls of blood vessels, which causes them to dilate or widen, reducing the resistance to blood flow and thereby lowering blood pressure. Verapamil also slows down the conduction of electrical signals within the heart, which can help to regulate the heart rate and rhythm.
In addition to its cardiovascular effects, verapamil is sometimes used off-label for the treatment of other conditions such as migraine headaches, Raynaud's phenomenon, and certain types of tremors. It is available in various forms, including immediate-release tablets, extended-release capsules, and intravenous (IV) injection.
It is important to note that verapamil can interact with other medications, so it is essential to inform your healthcare provider about all the drugs you are taking before starting this medication. Additionally, verapamil should be used with caution in people with certain medical conditions, such as heart failure, liver disease, and low blood pressure.
Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:
Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.
Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.
Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.
Dihydropyridines are a class of compounds that contain a core structure of two fused rings, each containing six carbon atoms, with a hydrogen atom attached to each of the two central carbon atoms. They are commonly used in pharmaceuticals, particularly as calcium channel blockers in the treatment of cardiovascular diseases.
Calcium channel blockers, including dihydropyridines, work by blocking the influx of calcium ions into cardiac and vascular smooth muscle cells. This leads to relaxation of the muscles, resulting in decreased peripheral resistance and reduced blood pressure. Dihydropyridines are known for their potent vasodilatory effects and include medications such as nifedipine, amlodipine, and felodipine.
It is important to note that while dihydropyridines can be effective in treating hypertension and angina, they may also have side effects such as headache, dizziness, and peripheral edema. Additionally, they may interact with other medications, so it is essential to consult a healthcare provider before starting or changing any medication regimen.
Calcium channels, L-type, are a type of voltage-gated calcium channel that are widely expressed in many excitable cells, including cardiac and skeletal muscle cells, as well as certain neurons. These channels play a crucial role in the regulation of various cellular functions, such as excitation-contraction coupling, hormone secretion, and gene expression.
L-type calcium channels are composed of five subunits: alpha-1, alpha-2, beta, gamma, and delta. The alpha-1 subunit is the pore-forming subunit that contains the voltage sensor and the selectivity filter for calcium ions. It has four repeated domains (I-IV), each containing six transmembrane segments (S1-S6). The S4 segment in each domain functions as a voltage sensor, moving outward upon membrane depolarization to open the channel and allow calcium ions to flow into the cell.
L-type calcium channels are activated by membrane depolarization and have a relatively slow activation and inactivation time course. They are also modulated by various intracellular signaling molecules, such as protein kinases and G proteins. L-type calcium channel blockers, such as nifedipine and verapamil, are commonly used in the treatment of hypertension, angina, and certain cardiac arrhythmias.
Calcium channels are specialized proteins that span the membrane of cells and allow calcium ions (Ca²+) to flow in and out of the cell. They are crucial for many physiological processes, including muscle contraction, neurotransmitter release, hormone secretion, and gene expression.
There are several types of calcium channels, classified based on their biophysical and pharmacological properties. The most well-known are:
1. Voltage-gated calcium channels (VGCCs): These channels are activated by changes in the membrane potential. They are further divided into several subtypes, including L-type, P/Q-type, N-type, R-type, and T-type. VGCCs play a critical role in excitation-contraction coupling in muscle cells and neurotransmitter release in neurons.
2. Receptor-operated calcium channels (ROCCs): These channels are activated by the binding of an extracellular ligand, such as a hormone or neurotransmitter, to a specific receptor on the cell surface. ROCCs are involved in various physiological processes, including smooth muscle contraction and platelet activation.
3. Store-operated calcium channels (SOCCs): These channels are activated by the depletion of intracellular calcium stores, such as those found in the endoplasmic reticulum. SOCCs play a critical role in maintaining calcium homeostasis and signaling within cells.
Dysregulation of calcium channel function has been implicated in various diseases, including hypertension, arrhythmias, migraine, epilepsy, and neurodegenerative disorders. Therefore, calcium channels are an important target for drug development and therapy.
I couldn't find a medical definition specifically for "delayed-action preparations." However, in the context of pharmacology, it may refer to medications or treatments that have a delayed onset of action. These are designed to release the active drug slowly over an extended period, which can help to maintain a consistent level of the medication in the body and reduce the frequency of dosing.
Examples of delayed-action preparations include:
1. Extended-release (ER) or controlled-release (CR) formulations: These are designed to release the drug slowly over several hours, reducing the need for frequent dosing. Examples include extended-release tablets and capsules.
2. Transdermal patches: These deliver medication through the skin and can provide a steady rate of drug delivery over several days. Examples include nicotine patches for smoking cessation or fentanyl patches for pain management.
3. Injectable depots: These are long-acting injectable formulations that slowly release the drug into the body over weeks to months. An example is the use of long-acting antipsychotic injections for the treatment of schizophrenia.
4. Implantable devices: These are small, biocompatible devices placed under the skin or within a body cavity that release a steady dose of medication over an extended period. Examples include hormonal implants for birth control or drug-eluting stents used in cardiovascular procedures.
Delayed-action preparations can improve patient compliance and quality of life by reducing dosing frequency, minimizing side effects, and maintaining consistent therapeutic levels.
Gingival overgrowth, also known as gingival hyperplasia or hypertrophy, refers to an abnormal enlargement or growth of the gum tissue (gingiva) surrounding the teeth. This condition can be caused by various factors, including poor oral hygiene, certain medications (such as phenytoin, cyclosporine, and calcium channel blockers), genetic predisposition, and systemic conditions like vitamin C deficiency or leukemia.
Gingival overgrowth can lead to several complications, such as difficulty in maintaining oral hygiene, which may result in periodontal disease, tooth decay, bad breath, and potential loss of teeth. In some cases, the enlarged gum tissue may also cause discomfort or pain during speaking, chewing, or brushing. Treatment for gingival overgrowth typically involves improving oral hygiene, adjusting medications if possible, and undergoing surgical procedures to remove the excess gum tissue. Regular dental check-ups and cleanings are essential in managing and preventing this condition.
Nicardipine is a medication that belongs to a class of drugs called calcium channel blockers. It works by relaxing the muscles of your heart and blood vessels, which helps to lower your blood pressure and increase the supply of oxygen and blood to your heart.
Medically, Nicardipine is defined as a dihydropyridine calcium antagonist that is used in the management of hypertension and angina pectoris. It selectively inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle cells, which leads to vasodilation and decreased peripheral resistance. Nicardipine also reduces afterload and myocardial oxygen demand, making it useful in the treatment of hypertension and angina pectoris. It is available in immediate-release and extended-release formulations for oral administration, as well as in an intravenous formulation for use in hospital settings.
Calcium channel agonists are substances that increase the activity or function of calcium channels. Calcium channels are specialized proteins in cell membranes that regulate the flow of calcium ions into and out of cells. They play a crucial role in various physiological processes, including muscle contraction, hormone secretion, and nerve impulse transmission.
Calcium channel agonists can enhance the opening of these channels, leading to an increased influx of calcium ions into the cells. This can result in various pharmacological effects, depending on the type of cell and tissue involved. For example, calcium channel agonists may be used to treat conditions such as hypotension (low blood pressure) or heart block by increasing cardiac contractility and heart rate. However, these agents should be used with caution due to their potential to cause adverse effects, including increased heart rate, hypertension, and arrhythmias.
Examples of calcium channel agonists include drugs such as Bay K 8644, FPL 64176, and A23187. It's important to note that some substances can act as both calcium channel agonists and antagonists, depending on the dose, concentration, or duration of exposure.
Tocolytic agents are a type of medication used in obstetrics to suppress premature labor. They work by relaxing the smooth muscle of the uterus, thereby reducing contractions and delaying delivery. Commonly used tocolytic agents include beta-adrenergic agonists (such as terbutaline), calcium channel blockers (such as nifedipine), and prostaglandin synthesis inhibitors (such as indomethacin). It's important to note that the use of tocolytic agents is typically reserved for specific clinical situations, and their benefits must be weighed against potential risks to both the mother and fetus.
Atenolol is a beta-blocker medication that is primarily used to treat hypertension (high blood pressure), angina (chest pain), and certain types of heart rhythm disorders. It works by blocking the action of certain hormones in the body, such as adrenaline, on the heart and blood vessels. This helps to reduce the heart's workload, lower its rate and force of contractions, and improve blood flow.
Beta-blockers like atenolol are also sometimes used to prevent migraines or to treat symptoms of anxiety, such as rapid heartbeat or tremors. Atenolol is available in immediate-release and extended-release forms, and it is typically taken orally once or twice a day. As with any medication, atenolol can have side effects, including dizziness, fatigue, and gastrointestinal symptoms, and it may interact with other medications or medical conditions. It is important to use atenolol only under the supervision of a healthcare provider.
Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:
1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.
Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.
Sublingual administration refers to a route of delivering medication or other substances through placement under the tongue, allowing for rapid absorption into the bloodstream through the mucous membranes located there. This method can allow for quick onset of action and avoids first-pass metabolism in the liver that may occur with oral administration. Common examples of sublingual medications include nitroglycerin for angina pectoris and certain forms of hormone replacement therapy.
Muscle contraction is the physiological process in which muscle fibers shorten and generate force, leading to movement or stability of a body part. This process involves the sliding filament theory where thick and thin filaments within the sarcomeres (the functional units of muscles) slide past each other, facilitated by the interaction between myosin heads and actin filaments. The energy required for this action is provided by the hydrolysis of adenosine triphosphate (ATP). Muscle contractions can be voluntary or involuntary, and they play a crucial role in various bodily functions such as locomotion, circulation, respiration, and posture maintenance.
Vasodilator agents are pharmacological substances that cause the relaxation or widening of blood vessels by relaxing the smooth muscle in the vessel walls. This results in an increase in the diameter of the blood vessels, which decreases vascular resistance and ultimately reduces blood pressure. Vasodilators can be further classified based on their site of action:
1. Systemic vasodilators: These agents cause a generalized relaxation of the smooth muscle in the walls of both arteries and veins, resulting in a decrease in peripheral vascular resistance and preload (the volume of blood returning to the heart). Examples include nitroglycerin, hydralazine, and calcium channel blockers.
2. Arterial vasodilators: These agents primarily affect the smooth muscle in arterial vessel walls, leading to a reduction in afterload (the pressure against which the heart pumps blood). Examples include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and direct vasodilators like sodium nitroprusside.
3. Venous vasodilators: These agents primarily affect the smooth muscle in venous vessel walls, increasing venous capacitance and reducing preload. Examples include nitroglycerin and other organic nitrates.
Vasodilator agents are used to treat various cardiovascular conditions such as hypertension, heart failure, angina, and pulmonary arterial hypertension. It is essential to monitor their use carefully, as excessive vasodilation can lead to orthostatic hypotension, reflex tachycardia, or fluid retention.
Omega-Conotoxin GVIA is a specific type of conotoxin, a peptide toxin derived from the venom of marine cone snails. This particular variant comes from the Conus geographus species.
Omega-Conotoxins are known for their ability to block N-type voltage-gated calcium channels (VGCCs). In the case of omega-Conotoxin GVIA, it specifically and potently inhibits N-type VGCCs, which play crucial roles in neurotransmitter release and pain signaling. Therefore, it has been extensively studied as a research tool to understand these channels' functions and as a potential lead compound for developing novel therapeutics, particularly for treating chronic pain conditions.
Felodipine is a medication that belongs to a class of drugs called calcium channel blockers. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve blood flow. Felodipine is commonly used to treat high blood pressure (hypertension) and angina (chest pain).
The medical definition of Felodipine is:
A dihydropyridine calcium channel blocker used in the treatment of hypertension and angina pectoris. It is a racemic mixture of two enantiomers, with the levo-isomer being more potent than the dextro-isomer. Felodipine lowers blood pressure by reducing peripheral vascular resistance through the inhibition of calcium ion influx into vascular smooth muscle cells.
Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.
Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.
If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.
Mibefradil is a medication that was previously used to treat hypertension (high blood pressure) and angina (chest pain due to reduced blood flow to the heart muscle). It belongs to a class of drugs known as calcium channel blockers, which work by relaxing the muscles of the blood vessels and increasing the supply of blood and oxygen to the heart while reducing its workload.
Mibefradil was first approved for medical use in 1997 but was later withdrawn from the market in 1998 due to its interactions with several other medications, which could lead to dangerous side effects. Currently, it is not available for medical use.
A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.
The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.
The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.
In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.
Smooth muscle, also known as involuntary muscle, is a type of muscle that is controlled by the autonomic nervous system and functions without conscious effort. These muscles are found in the walls of hollow organs such as the stomach, intestines, bladder, and blood vessels, as well as in the eyes, skin, and other areas of the body.
Smooth muscle fibers are shorter and narrower than skeletal muscle fibers and do not have striations or sarcomeres, which give skeletal muscle its striped appearance. Smooth muscle is controlled by the autonomic nervous system through the release of neurotransmitters such as acetylcholine and norepinephrine, which bind to receptors on the smooth muscle cells and cause them to contract or relax.
Smooth muscle plays an important role in many physiological processes, including digestion, circulation, respiration, and elimination. It can also contribute to various medical conditions, such as hypertension, gastrointestinal disorders, and genitourinary dysfunction, when it becomes overactive or underactive.
I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).
In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.
Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.
Angina pectoris is a medical term that describes chest pain or discomfort caused by an inadequate supply of oxygen-rich blood to the heart muscle. This condition often occurs due to coronary artery disease, where the coronary arteries become narrowed or blocked by the buildup of cholesterol, fatty deposits, and other substances, known as plaques. These blockages can reduce blood flow to the heart, causing ischemia (lack of oxygen) and leading to angina symptoms.
There are two primary types of angina: stable and unstable. Stable angina is predictable and usually occurs during physical exertion or emotional stress when the heart needs more oxygen-rich blood. The pain typically subsides with rest or after taking prescribed nitroglycerin medication, which helps widen the blood vessels and improve blood flow to the heart.
Unstable angina, on the other hand, is more severe and unpredictable. It can occur at rest, during sleep, or with minimal physical activity and may not be relieved by rest or nitroglycerin. Unstable angina is considered a medical emergency, as it could indicate an imminent heart attack.
Symptoms of angina pectoris include chest pain, pressure, tightness, or heaviness that typically radiates to the left arm, neck, jaw, or back. Shortness of breath, nausea, sweating, and fatigue may also accompany angina symptoms. Immediate medical attention is necessary if you experience chest pain or discomfort, especially if it's new, severe, or persistent, as it could be a sign of a more serious condition like a heart attack.
A smooth muscle within the vascular system refers to the involuntary, innervated muscle that is found in the walls of blood vessels. These muscles are responsible for controlling the diameter of the blood vessels, which in turn regulates blood flow and blood pressure. They are called "smooth" muscles because their individual muscle cells do not have the striations, or cross-striped patterns, that are observed in skeletal and cardiac muscle cells. Smooth muscle in the vascular system is controlled by the autonomic nervous system and by hormones, and can contract or relax slowly over a period of time.
I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."
In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.
Tocolysis is a medical intervention used to suppress preterm labor. It involves the use of medications that aim to relax the uterus and stop contractions, thereby delaying or preventing preterm delivery. The goal of tocolysis is to give time for corticosteroid administration to promote fetal lung maturity and allow for the transfer of the mother to a facility with a higher level of neonatal care, if necessary. Commonly used tocolytic agents include calcium channel blockers, beta-adrenergic agonists, and nitric oxide donors. It's important to note that tocolysis is not always successful in preventing preterm birth, and its use should be carefully considered based on the individual circumstances and gestational age of the pregnancy.
Potassium chloride is an essential electrolyte that is often used in medical settings as a medication. It's a white, crystalline salt that is highly soluble in water and has a salty taste. In the body, potassium chloride plays a crucial role in maintaining fluid and electrolyte balance, nerve function, and muscle contraction.
Medically, potassium chloride is commonly used to treat or prevent low potassium levels (hypokalemia) in the blood. Hypokalemia can occur due to various reasons such as certain medications, kidney diseases, vomiting, diarrhea, or excessive sweating. Potassium chloride is available in various forms, including tablets, capsules, and liquids, and it's usually taken by mouth.
It's important to note that potassium chloride should be used with caution and under the supervision of a healthcare provider, as high levels of potassium (hyperkalemia) can be harmful and even life-threatening. Hyperkalemia can cause symptoms such as muscle weakness, irregular heartbeat, and cardiac arrest.
"Gallopamil" is not a recognized medical term or a medication in current use. It may be a misspelling or a misunderstanding of "Gallopamil," which is the international nonproprietary name (INN) for a pharmaceutical drug known as "Diltiazem."
Diltiazem is a calcium channel blocker, a type of medication used to treat high blood pressure, angina (chest pain), and certain heart rhythm disorders. It works by relaxing the muscles of the blood vessels and slowing down the heart rate, which can help reduce the force and frequency of heart contractions and improve blood flow.
It's important to note that medications should always be taken under the guidance and supervision of a healthcare professional, who can provide accurate information about their intended uses, potential side effects, and appropriate dosages based on individual patient needs.
Amlodipine is a type of medication known as a calcium channel blocker, which is primarily used to treat high blood pressure and angina (chest pain caused by reduced blood flow to the heart). It works by relaxing the muscles around the blood vessels, which causes them to widen and improves blood flow. This helps to lower blood pressure and reduce the workload on the heart, making it easier for the heart to pump blood effectively.
Amlodipine is available in various strengths as a tablet or an extended-release tablet, and it is typically taken once daily. The medication may take several weeks to reach its full effect, so it is important to continue taking it even if you do not notice any immediate improvement in your symptoms.
As with any medication, amlodipine can cause side effects, including headache, dizziness, fatigue, and swelling of the ankles or feet. In rare cases, it may also cause more serious side effects such as allergic reactions, irregular heartbeat, or liver damage. If you experience any unusual symptoms while taking amlodipine, it is important to contact your healthcare provider right away.
It is important to follow your healthcare provider's instructions carefully when taking amlodipine, and to inform them of any other medications or supplements that you are taking, as well as any medical conditions that you have. This will help ensure that the medication is safe and effective for you to use.
Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.
A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:
1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.
It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.
Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:
1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.
The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.
Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.
Nitrendipine is an antihypertensive drug, which belongs to the class of calcium channel blockers. It works by relaxing and widening the blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system. This helps to lower high blood pressure (hypertension) and improve overall cardiovascular health. Nitrendipine is available in oral tablet form and is typically prescribed by a healthcare professional for the treatment of hypertension.
It's important to note that this definition is intended to be a general overview of the medical use and properties of Nitrendipine, and it should not be used as a substitute for professional medical advice or treatment. Always consult with a qualified healthcare provider for information regarding any specific medical condition or treatment.
The double-blind method is a study design commonly used in research, including clinical trials, to minimize bias and ensure the objectivity of results. In this approach, both the participants and the researchers are unaware of which group the participants are assigned to, whether it be the experimental group or the control group. This means that neither the participants nor the researchers know who is receiving a particular treatment or placebo, thus reducing the potential for bias in the evaluation of outcomes. The assignment of participants to groups is typically done by a third party not involved in the study, and the codes are only revealed after all data have been collected and analyzed.
Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.
As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.
In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.
Nisoldipine is a dihydropyridine calcium channel blocker that is primarily used in the management of hypertension (high blood pressure) and angina pectoris (chest pain due to reduced blood flow to the heart muscle). It works by relaxing and dilating the smooth muscles of blood vessels, which improves blood flow and reduces the workload on the heart.
Nisoldipine inhibits the influx of calcium ions into vascular smooth muscle cells and cardiac muscle cells, leading to a decrease in intracellular calcium concentrations. This results in the relaxation of vascular smooth muscle, which causes vasodilation and decreases peripheral resistance, thereby reducing blood pressure.
Nisoldipine is available in oral form as extended-release tablets and is typically administered once or twice daily. The most common side effects include headache, dizziness, flushing, peripheral edema (swelling of the legs and ankles), and palpitations. It is important to note that Nisoldipine should be used with caution in patients with hepatic impairment, and its use should be avoided in patients with severe aortic stenosis or unstable angina pectoris.
Cytochrome P-450 CYP3A is a subfamily of the cytochrome P-450 enzyme superfamily, which are primarily involved in drug metabolism in the human body. These enzymes are found predominantly in the liver, but also in other tissues such as the small intestine, kidneys, and brain.
CYP3A enzymes are responsible for metabolizing a wide variety of drugs, including many statins, benzodiazepines, antidepressants, and opioids. They can also metabolize endogenous compounds such as steroids and bile acids. The activity of CYP3A enzymes can be influenced by various factors, including genetic polymorphisms, age, sex, pregnancy, and the presence of other drugs or diseases.
The name "cytochrome P-450" refers to the fact that these enzymes contain a heme group that absorbs light at a wavelength of 450 nanometers when it is complexed with carbon monoxide. The term "CYP3A" denotes the specific subfamily of cytochrome P-450 enzymes that share a high degree of sequence similarity and function.
Ryanodine is not a medical condition or term, but it is a chemical compound that interacts with ryanodine receptors (RyRs), which are calcium release channels found in the sarcoplasmic reticulum of muscle cells. Ryanodine receptors play a crucial role in excitation-contraction coupling, which is the process by which electrical signals trigger muscle contractions.
Ryanodine itself is a plant alkaloid that was initially isolated from the South American shrub Ryania speciosa. It can bind to and inhibit ryanodine receptors, altering calcium signaling in muscle cells. This ability of ryanodine to modulate calcium release has made it a valuable tool in researching excitation-contraction coupling and related processes.
In some cases, the term "ryanodine" may be used in a medical context to refer to the effects of ryanodine or ryanodine receptor modulation on muscle function, particularly in relation to diseases associated with calcium handling abnormalities. However, it is not a medical condition per se.
Isradipine is a medication that belongs to a class of drugs called calcium channel blockers. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve the supply of oxygen and nutrients to the heart. Isradipine is used to treat high blood pressure (hypertension) and angina (chest pain).
The medical definition of Isradipine is:
A dihydropyridine calcium channel blocker, which is a selective inhibitor of calcium ion influx through the slow channels of cardiac and vascular muscle and is used in the treatment of hypertension and angina pectoris. The drug has positive inotropic effects on the heart and increases coronary blood flow. It has a rapid onset of action and a short elimination half-life, making it useful for the control of acute hypertensive episodes.
Antihypertensive agents are a class of medications used to treat high blood pressure (hypertension). They work by reducing the force and rate of heart contractions, dilating blood vessels, or altering neurohormonal activation to lower blood pressure. Examples include diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers, and direct vasodilators. These medications may be used alone or in combination to achieve optimal blood pressure control.
Vasoconstriction is a medical term that refers to the narrowing of blood vessels due to the contraction of the smooth muscle in their walls. This process decreases the diameter of the lumen (the inner space of the blood vessel) and reduces blood flow through the affected vessels. Vasoconstriction can occur throughout the body, but it is most noticeable in the arterioles and precapillary sphincters, which control the amount of blood that flows into the capillary network.
The autonomic nervous system, specifically the sympathetic division, plays a significant role in regulating vasoconstriction through the release of neurotransmitters like norepinephrine (noradrenaline). Various hormones and chemical mediators, such as angiotensin II, endothelin-1, and serotonin, can also induce vasoconstriction.
Vasoconstriction is a vital physiological response that helps maintain blood pressure and regulate blood flow distribution in the body. However, excessive or prolonged vasoconstriction may contribute to several pathological conditions, including hypertension, stroke, and peripheral vascular diseases.
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Tablets7
- Nifedipine extended-release tablets are an extended-release tablet dosage form of the calcium channel blocker nifedipine. (nih.gov)
- Nifedipine extended-release tablets contain 30 mg of nifedipine for once-a-day oral administration. (nih.gov)
- Nifedipine extended-release tablets meet USP Dissolution Test 4 (using first derivative UV spectrophotometry at 245 nm for sample analysis). (nih.gov)
- After ingestion of nifedipine extended-release tablets under fasting conditions, plasma concentrations peak at about 2.5 to 5 hours with a second small peak or shoulder evident at approximately 6 to 12 hours post dose. (nih.gov)
- Two 30 mg nifedipine extended-release tablets may be interchanged with a 60 mg nifedipine extended-release tablet. (nih.gov)
- Three 30 mg nifedipine extended-release tablets, however, result in substantially higher C max values than those after a single 90 mg nifedipine extended-release tablet. (nih.gov)
- INDICATIONS: CHEMMART nifedipine tablets are indicated for the treatment of hypertension . (healthdirect.gov.au)
Calcium22
- Nifedipine, sold under the brand names Adalat and Procardia among others, is a calcium channel blocker medication used to manage angina, high blood pressure, Raynaud's phenomenon, and premature labor. (wikipedia.org)
- As calcium channel blocker, nifedipine has a risk of causing gingival hyperplasia A number of persons have developed toxicity due to acute overdosage with nifedipine, either accidentally or intentionally, and via either oral or parenteral administration. (wikipedia.org)
- Nifedipine is in a class of medications called calcium-channel blockers. (medlineplus.gov)
- Nifedipine is a calcium ion influx inhibitor (slow-channel blocker or calcium ion antagonist) which inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. (nih.gov)
- Nifedipine selectively inhibits calcium ion influx across the cell membrane of vascular smooth muscle and cardiac muscle without altering serum calcium concentrations. (nih.gov)
- The binding of nifedipine to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. (nih.gov)
- The reduction in calcium influx by nifedipine causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure. (nih.gov)
- Nifedipine is an antianginal drug belonging to a class of pharmacological agents, the calcium channel blockers. (nih.gov)
- The calcium antagonists diltiazem, nifedipine and verapamil are widely used in the treatment of coronary heart disease, arterial hypertension, certain supraventricular tachyarrhythmias and obstructive hypertrophic cardiomyopathy. (nih.gov)
- Amlodipine and Nifedipine are medications belonging to the group of calcium channel blockers primarily used to control high blood pressure. (differencebetween.net)
- Nifedipine is a short acting calcium channel blocker causing dilatation of the peripheral blood vessels. (differencebetween.net)
- NIFEDIPINE is a calcium-channel blocker. (somalinet.com)
- In order to assess the in vivo relevance of these data, we studied, in healthy volunteers, the influence of nifedipine, a calcium channel blocking agent, on the intestinal uptake of amoxicillin, a commonly prescribed and well-absorbed aminopenicillin. (aspetjournals.org)
- No changes in sensitivity to verapamil and nifedipine were recorded during the first month of postnatal development, thus suggesting that the function of calcium channels involved in the response to K^+ does not change during this period. (karger.com)
- In the APOSTEL III trial we aimed to compare the effectiveness and safety of the calcium-channel blocker nifedipine and the oxytocin inhibitor atosiban in women with threatened preterm birth. (monash.edu)
- Nifedipine is a calcium channel blocker that is also used in the management of hypertension at doses of 10 to 40 mg 2 times daily or 20 to 90 mg once daily, depending on the sustained-release form used. (msf.org)
- Information on Dihydropyridine Calcium Channel Blockers (CCBs): Amlodipine (Norvasc), Felodipine (Renedil, Plendil), Nifedipine (Adalat XL), used to prevent angina, treat high blood pressure, and reduce complications of high blood pressure such as heart attack and stroke. (eduhealth.ca)
- Nilol (Nifedipine/Atenolol) belongs to a class of medications called calcium channel blockers. (unitedpharmacies.com)
- Top, CPT increased MSA independently of treatment (§P. 67%) Amlodipine is a 3 rd generation calcium channel antagonist while Nifedipine is 1st generation calcium channel antagonist. (commercialpaintingusa.com)
- 001), however the clinical significance of the 4 beats/minute decrease with COER-verapamil as compared to the 2 beats per minute increase with nifedipine GITS is minimal Be aware: all the calcium channel blockers, except amlodipine (neutral), in outcome tracking databases, ↑ mortality. (commercialpaintingusa.com)
- Nifedipine is in a group of drugs called calcium channel blockers. (canadianfpharmacy.com)
- The Giant PANDA study is a pragmatic, open-label, multicentre, randomised controlled trial of a treatment initiation strategy with nifedipine ( calcium channel blocker ), versus labetalol (mixed alpha/beta blocker) in 2300 women with pregnancy hypertension . (bvsalud.org)
Metabolism1
- We conclude that concomitant use of V. amygdalina reduced the metabolism of nifedipine evident by decrease in clearance and increased F and AUC thus altering its pharmacokinetic profile. (phytojournal.com)
Pharmacokinetics3
- Since hepatic biotransformation is the predominant route for the disposition of nifedipine, the pharmacokinetics may be altered in patients with chronic liver disease. (nih.gov)
- Whereas renal disease has no impact on the pharmacokinetics of diltiazem and verapamil, elimination half-life of nifedipine increases in relation to the degree of renal impairment due to an increase in volume of distribution. (nih.gov)
- Owolabi, M A*., Adeniji, E A., Oribayo O O. And Akindehin O E.. Effects of Vernonia Amygdalina Aqueous Leaf Extract on the Pharmacokinetics of Nifedipine in Rabbits . (phytojournal.com)
Erectile dysfunction24
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Dizziness3
- Nifedipine may cause dizziness or lightheadedness. (somalinet.com)
- Nifedipine XR Side Effects can include dizziness, headache, or flushing. (novacorp.biz)
- Dizziness or lightheadedness is another potential side effect of using Nifedipine Xr. (novacorp.biz)
Dihydropyridine1
- Nifedipine is in the dihydropyridine class and the other two are not. (commercialpaintingusa.com)
Angina17
- Nifedipine is one of the main choices for the treatment of Prinzmetal angina due to its vasodilating effects on the coronary arteries. (wikipedia.org)
- Nifedipine is used to treat high blood pressure and to control angina (chest pain). (medlineplus.gov)
- Nifedipine controls high blood pressure and chest pain (angina) but does not cure them. (medlineplus.gov)
- This property increases myocardial oxygen delivery in patients with coronary artery spasm,and is responsible for the effectiveness of nifedipine in vasospastic (Prinzmetal's or variant) angina. (nih.gov)
- This unloading of the heart reduces myocardial energy consumption and oxygen requirements and probably accounts for the effectiveness of nifedipine in chronic stable angina. (nih.gov)
- Nifedipine is indicated for the management of vasospastic angina confirmed by any of the following criteria: 1) classical pattern of angina at rest accompanied by ST segment elevation, 2) angina or coronary artery spasm provoked by ergonovine, or 3) angiographically demonstrated coronary artery spasm. (rxlist.com)
- Nifedipine may also be used where the clinical presentation suggests a possible vasospastic component but where vasospasm has not been confirmed, e.g., where pain has a variable threshold on exertion or when angina is refractory to nitrates and/or adequate doses of beta blockers . (rxlist.com)
- Nifedipine is indicated for the management of chronic stable angina (effort-associated angina) without evidence of vasospasm in patients who remain symptomatic despite adequate doses of beta blockers and/or organic nitrates or who cannot tolerate those agents. (rxlist.com)
- In chronic stable angina (effort-associated angina) nifedipine has been effective in controlled trials of up to eight weeks duration in reducing angina frequency and increasing exercise tolerance, but confirmation of sustained effectiveness and evaluation of long-term safety in these patients are incomplete. (rxlist.com)
- Controlled studies in small numbers of patients suggest concomitant use of nifedipine and beta-blocking agents may be beneficial in patients with chronic stable angina, but available information is not sufficient to predict with confidence the effects of concurrent treatment, especially in patients with compromised left ventricular function or cardiac conduction abnormalities. (rxlist.com)
- Both Amlodipine and Nifedipine are also used to control angina, chest discomfort due to lack of blood supply to the heart. (differencebetween.net)
- Just like amlodipine nifedipine is also never used for ongoing angina. (differencebetween.net)
- Amlodipine and Nifedipine both are used to control high blood pressure and angina. (differencebetween.net)
- So all in all, its quite evident that an women with angina, but it may not be the (sternum) and Nifedipine rush Order open your ribcage to reach your. (altabhossainptti.org)
- They are stable angina and acute coronary Nifedipine rush Order. (altabhossainptti.org)
- Nifedipine XR, also referred to as extended-release nifedipine, is a commonly prescribed medication for managing high blood pressure and angina. (novacorp.biz)
- Nifedipine is a medication used to manage angina, high blood pressure, Raynaud's phenomenon, and premature labor. (xenexlabs.us)
Take nifedipine5
- To help you remember to take nifedipine, take it at around the same time(s) every day. (medlineplus.gov)
- Take nifedipine exactly as directed. (medlineplus.gov)
- Continue to take nifedipine even if you feel well. (medlineplus.gov)
- Can I take Nifedipine (Chemmart) in sport? (healthdirect.gov.au)
- Take Nifedipine by mouth with or without food. (somalinet.com)
Blood nifedipine1
- medical citation needed] Extended release formulations of nifedipine should be taken on an empty stomach, and patients are warned not to consume anything containing grapefruit or grapefruit juice, as they raise blood nifedipine levels. (wikipedia.org)
Effects of nifedipine1
- One of the commonly experienced side effects of Nifedipine Xr is facial flushing or a reddening of the skin. (novacorp.biz)
Verapamil9
- The effects of verapamil and nifedipine on K+-induced contractions were studied in the isolated ileum of newborn, 30-day-old and adult guinea pigs. (karger.com)
- Both verapamil and nifedipine inhibited the K+-induced contractions, with nifedipine demonstrating the highest activity. (karger.com)
- Verapamil reduced mean diastolic blood pressure significantly more than nifedipine in all positions and lowered mean systolic pressure slightly more than nifedipine. (commercialpaintingusa.com)
- This fall occurred within 20-30 minutes of the oral ingestion of 20 mg of nifedipine, and the effect lasted for another 30 minutes Verapamil (2-20 μM), diltiazem (22-814 μM) and nifedipine (29-896 μM) produced concentration-dependent relaxation of human isolated saphenous vein. (commercialpaintingusa.com)
- Verapamil and diltiazem difference between verapamil and nifedipine cause a significant increase in plasma digoxin concentrations. (commercialpaintingusa.com)
- There was a significantly greater fall in systolic blood pressure on nifedipine (23 mm Hg) compared with verapamil (13 mm Hg) (P less than 0. (commercialpaintingusa.com)
- The animals were injected with 1 mg kg-1 nifedipine (F) or 5 mg kg-1 verapamil (V) or difference between verapamil and nifedipine an equivalent volume of the vehicle (H) (Cremophor EL), i. (commercialpaintingusa.com)
- Nifedipine doesn't affect conduction but the other 2 do Verapamil Nifedipine (verapamil-nifedipine) n n Asignificant difference between thetwotreatmentswasfoundforthe complaint rate (P2 years ago VAS scores for bleeding in the Nifedipine group ( P = 0. (commercialpaintingusa.com)
- This fall occurred within 20-30 minutes of the oral ingestion of 20 mg of nifedipine, and the effect lasted for difference between verapamil and nifedipine another 30 minutes The mean decrease in SBP was 18. (commercialpaintingusa.com)
Preterm3
- Nifedipine is also used sometimes to treat preterm labor and Raynaud's syndrome. (medlineplus.gov)
- Women with threatened preterm birth (gestational age 25-34 weeks) were randomly assigned (1:1) to either oral nifedipine or intravenous atosiban for 48 h. (monash.edu)
- Interpretation In women with threatened preterm birth, 48 h of tocolysis with nifedipine or atosiban results in similar perinatal outcomes. (monash.edu)
Hypertension4
- An exception to the avoidance of this practice is in the use of nifedipine for the treatment of hypertension associated with autonomic dysreflexia in spinal cord injury. (wikipedia.org)
- Immediate-release forms of nifedipine should not be used in either long-term treatment of hypertension or treatment of hypertensive crisis (risk of excessive fall in blood pressure and cerebral or myocardial ischaemia in patients with coronary artery disease). (msf.org)
- A treatment strategy with nifedipine versus labetalol for women with pregnancy hypertension: study protocol for a randomised controlled trial (Giant PANDA). (bvsalud.org)
- The primary objective is to evaluate if treatment with nifedipine compared to labetalol in women with pregnancy hypertension reduces severe maternal hypertension without increasing fetal or neonatal death or neonatal unit admission. (bvsalud.org)
Pregnancy2
- Nifedipine is considered safe in pregnancy and breastfeeding. (wikipedia.org)
- Nifedipine is contraindicated in patients with severe heart disease, kidney or liver disease, heart failure, blockage in digestive tract, history of stomach surgery, lung disease, in pregnancy, and during breast feeding. (differencebetween.net)
Chest4
- If taken regularly, nifedipine controls chest pain, but it does not stop chest pain once it starts. (medlineplus.gov)
- Stop nifedipine if ischaemic chest pain occurs or existing pain increases after starting treatment. (msf.org)
- Nifedipine Xr is a commonly prescribed drug used to treat high blood pressure and specific types of chest pain. (novacorp.biz)
- In conclusion, while Nifedipine Xr effectively manages high blood pressure and chest pain, it is crucial to familiarize oneself with its possible side effects. (novacorp.biz)
Capsule2
- Nifedipine comes as a capsule and an extended-release (long-acting) tablet to take by mouth. (medlineplus.gov)
- The elimination half-life of nifedipine administered as nifedipine extended-release tablet is approximately 7 hours in contrast to the known 2 hour elimination half-life of nifedipine administered as an immediate-release capsule. (nih.gov)
Bioavailability3
- There is little difference in relative bioavailability when nifedipine capsules are given orally and either swallowed whole, bitten and swallowed, or bitten and held sublingually. (nih.gov)
- Patients with hepatic impairment (liver cirrhosis) have a longer disposition half-life and higher bioavailability of nifedipine than healthy volunteers. (nih.gov)
- Nifedipine enhances amoxicillin absorption kinetics and bioavailability in humans. (aspetjournals.org)
Phenytoin5
- Monitor combination with cimetidine (enhances hypotensive effects), phenytoin (risk of phenytoin overdose), rifampicin (efficacy of nifedipine diminished), itraconazole (increased risk of oedema), beta-blockers (increased adverse cardiac effects). (msf.org)
- The aim of this study was to evaluate the prevalence of drug-induced gingival overgrowth (DIGO) in Brazilian users of nifedipine and/or phenytoin and to determine the presence of predisposing/modifying factors. (bvsalud.org)
- Demographic, pharmacological, and periodontal data were obtained from 100 users of the Brazilian Primary Health Care System in Diamantina, Jequitinhonha Valley, Minas Gerais state, Brazil, who were taking nifedipine and/or phenytoin. (bvsalud.org)
- The prevalence of DIGO was significantly higher in phenytoin users than in nifedipine users ( p =0.01). (bvsalud.org)
- The high occurrence of DIGO among users of nifedipine and phenytoin emphasizes the importance of the dentist as part of the public health team to provide the prevention, early diagnostic, and control of this alteration. (bvsalud.org)
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Myocardial infarction2
- There have been multiple reports in the medical literature of serious adverse effects with sublingual nifedipine, including cerebral ischemia/infarction, myocardial infarction, complete heart block, and death. (wikipedia.org)
- Any myocardial infarction or stroke followed by death, whatever in both women and men, Nifedipine Rush Order , but many people dont and what can bring relief. (altabhossainptti.org)
Prescription1
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Generic8
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Anal1
- Topical nifedipine has been shown to be as effective as topical nitrates for anal fissures. (wikipedia.org)
Reduces3
- The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilatation and, consequently, a reduction in peripheral vascular resistance. (nih.gov)
- Nifedipine regularly reduces arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing the total peripheral resistance (afterload) against which the heart works. (nih.gov)
- Necropolis of Action: The circumstance by which nifedipine reduces standardized blood pressure On Fri, 12 Dec 2003, in rec. (00it.com)
Grapefruit juice1
- Do not eat grapefruit or drink grapefruit juice while you use Nifedipine. (somalinet.com)
Medications1
- tell your doctor and pharmacist if you are allergic to nifedipine, any other medications, or any of the ingredients in nifedipine. (medlineplus.gov)
Arterial2
- Nifedipine is a peripheral arterial vasodilator which acts directly on vascular smooth muscle. (nih.gov)
- Before taking Nilol (Nifedipine/Atenolol), inform your physician if you have any arterial circulatory disorders, impaired renal function, hepatic renal function, carcinogenesis, mutagenesis, or impairment of fertility. (unitedpharmacies.com)
Amlodipine3
- It is seen that patients on nifedipine suffer more side effects as compared to those on amlodipine. (differencebetween.net)
- The mechanism through which both of these act is the same but while amlodipine is long acting and nifedipine is a short acting medicine. (differencebetween.net)
- Amlodipine is preferred for long term use in controlling high blood pressure since nifedipine is seen to cause more number of side effects. (differencebetween.net)
Medication1
- While Nifedipine XR can be an effective treatment for certain conditions, it is essential to be aware of its potential side effects and to stay vigilant in monitoring any changes in one's health while on this medication. (novacorp.biz)
Elimination1
- Nifedipine decreases the elimination of digoxin (Lanoxin) by the kidneys which increases digoxin toxicity. (modafinia.com)
Digoxin2
- In contrast, nifedipine does not lead to a significant increase in the plasma digoxin concentration. (nih.gov)
- The mechanism responsible for this interaction is inhibition of both renal and non-renal digoxin clearance They found a drop in LES pressure in all subjects given nifedipine, the mean LES pressure falling from 17. (commercialpaintingusa.com)
Vasodilation1
- Sublingual administration of nifedipine promotes a hypotensive effect via peripheral vasodilation. (wikipedia.org)
Coronary3
- Nifedipine dilates the main coronary arteries and coronary arterioles, both in normal and ischemic regions, and is a potent inhibitor of coronary artery spasm, whether spontaneous or ergonovine-induced. (nih.gov)
- Treatment of coronary heart disease depends on Nifedipine rushes Order results and the cause of your coronary heart disease. (altabhossainptti.org)
- Before taking nifedipine, tell your doctor if you have kidney or liver disease (especially cirrhosis), coronary artery disease, congestive heart failure, or digestive problems. (canadianfpharmacy.com)
Significantly1
- Based on screening diagnostic criteria, if you have the CAC significantly improves risk prediction and Nifedipine rush Order compared to future heart events. (altabhossainptti.org)
Raynaud's2
- Raynaud's phenomenon is often treated with nifedipine. (wikipedia.org)
- Nifedipine is used for other purposes too such as in pre-term labour and in Raynaud's phenomenon (discoloration of fingers and toes due to reduced blood supply as a response to cold and emotional stress). (differencebetween.net)
Doses2
- it does conclude that most included studies used low doses of nifedipine. (wikipedia.org)
- Nifedipine rapidly lowers blood pressure, and patients are commonly warned they may feel dizzy or faint after taking the first few doses. (wikipedia.org)
Allergic1
- You should not use nifedipine if you are allergic to it. (canadianfpharmacy.com)
Capsules1
- Nifedipine capsules are formulated as soft gelatin capsules for oral administration each containing 10 mg nifedipine. (nih.gov)
Atenolol1
- The recommended initial dose is 50mg of Nilol (Nifedipine/Atenolol), and this may be increased up to 100mg per day. (unitedpharmacies.com)
Sustained-release1
- These problems are much less frequent in the sustained-release preparations of nifedipine. (wikipedia.org)
Dose1
- Your doctor will probably start you on a low dose of nifedipine and gradually increase your dose, generally once every 7 to 14 days. (medlineplus.gov)
Kidneys1
- Nifedipine is extensively converted to inactive metabolites and approximately 80 percent of nifedipine and metabolites are eliminated via the kidneys. (nih.gov)