Potassium channel blockers are agents which interfere with conduction through potassium channels. Potassium channel blockers used in the treatment of cardiac arrhythmia are classified as class III antiarrhythmic agents. Class III agents predominantly block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channelconduction velocity is not decreased.

The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. The re-entrant rhythm is less likely to interact with tissue that has become refractory. These agents include a risk of torsades de pointes.

Sulfonylureassuch as gliclazideare ATP-sensitive potassium channel blockers. DalfampridineA potassium channel blocker has also been approved for use in the treatment of multiple sclerosis. Potassium channel blockers exhibit reverse use-dependent prolongation of the action potential duration. Reverse use dependence is the effect where the efficacy of the drug is reduced after repeated use of the tissue.

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Reverse use dependence is relevant for potassium channel blockers used as class III antiarrhythmics. Reverse use dependent drugs that slow heart rate such as quinidine can be less effective at high heart rates. Drugs such as quinidine may be both reverse use dependent and use dependent.

Examples of calcium-activated channel blockers include:. Examples of inwardly rectifying channel blockers include:. Examples of tandem pore domain channel blockers include:. Examples of voltage-gated channel blockers include:. From Wikipedia, the free encyclopedia.

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Unsourced material may be challenged and removed. Meglitinides Non- Sulfonylureas Mitiglinide Nateglinide Repaglinide Sulfonylureas Acetohexamide [ citation needed ] Carbutamide [ citation needed ] Chlorpropamide [ citation needed ] Glycyclamide Metahexamide Sulfonylureas continued Tolazamide Tolbutamide Glibornuride [ citation needed ] Glisoxepide Glyclopyramide Gliclazide [28] Glibenclamide glyburide [29] [12] Glipizide [ citation needed ] Glimepiride [ citation needed ] Glicaramide [ citation needed ].

This section needs additional citations for verification. May Learn how and when to remove this template message. Cardiol J. John; Shenasa, Mohammad eds. Biophysical Journal.

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Bibcode : BpJ Acta Pharmacologica Sinica.Calcium channel blockers lower your blood pressure by preventing calcium from entering the cells of your heart and arteries. Calcium causes the heart and arteries to contract more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open. Some calcium channel blockers have the added benefit of slowing your heart rate, which can further lower your blood pressure, relieve chest pain angina and control an irregular heartbeat.

Medically reviewed by Drugs. Last updated on Sep 19, Calcium channel blockers are available in short-acting and long-acting forms. Short-acting medications work quickly, but their effects last only a few hours.

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Long-acting medications are slowly released to provide a longer lasting effect. Several calcium channel blockers are available.

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Which one is best for you depends on your health and the condition being treated. In some cases, your doctor might prescribe a calcium channel blocker with other high blood pressure medications or with cholesterol-lowering drugs such as statins. In addition to high blood pressure, doctors prescribe calcium channel blockers to prevent, treat or improve symptoms in a variety of conditions, such as:.

For black people and older people, calcium channel blockers might work better than other blood pressure medications, such as beta blockers, angiotensin-converting enzyme ACE inhibitors or angiotensin II receptor blockers. Avoid grapefruit products while taking certain calcium channel blockers.

Grapefruit juice interacts with the drug and can affect heart rate and blood pressure. This can cause symptoms such as headaches and dizziness.

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Potassium-Channel Openers

This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment. Skip to Content. Calcium channel blockers On this page Examples of calcium channel blockers When calcium channel blockers are used Side effects Calcium channel blockers lower your blood pressure by preventing calcium from entering the cells of your heart and arteries.

Calcium channel blockers are also called calcium antagonists. Examples of calcium channel blockers Calcium channel blockers are available in short-acting and long-acting forms.

Examples of calcium channel blockers include: Amlodipine Norvasc Diltiazem Cardizem, Tiazac, others Felodipine Isradipine Nicardipine Nifedipine Adalat CC, Procardia Nisoldipine Sular Verapamil Calan, Verelan In some cases, your doctor might prescribe a calcium channel blocker with other high blood pressure medications or with cholesterol-lowering drugs such as statins.

When calcium channel blockers are used In addition to high blood pressure, doctors prescribe calcium channel blockers to prevent, treat or improve symptoms in a variety of conditions, such as: Coronary artery disease Chest pain angina Irregular heartbeats arrhythmia Some circulatory conditions, such as Raynaud's disease For black people and older people, calcium channel blockers might work better than other blood pressure medications, such as beta blockers, angiotensin-converting enzyme ACE inhibitors or angiotensin II receptor blockers.

Side effects Side effects of calcium channel blockers may include: Constipation Dizziness Fast heartbeat palpitations Fatigue Flushing Headache Nausea Rash Swelling in the feet and lower legs Avoid grapefruit products while taking certain calcium channel blockers. Recently Approved.

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Klabunde Sodium-channel blockers comprise the Class I antiarrhythmic compounds according to the Vaughan-Williams classification scheme. These drugs bind to and block the fast sodium channels that are responsible for the rapid depolarization phase 0 of fast-response cardiac action potentials. This type of action potential is found in non-nodal, cardiomyocytes e.

In contrast, nodal tissue action potentials sinoatrial and atrioventricular nodes do not depend on fast sodium channels for depolarization; instead, phase 0 depolarization is carried by calcium currents. Therefore, sodium-channel blockers have no direct effect on nodal tissue, at least through the blockade of fast sodium-channels. The principal effect of reducing the rate and magnitude of depolarization by blocking sodium channels is a decrease in conduction velocity in non-nodal tissue atrial and ventricular muscle, purkinje conducting system.

The faster a cell depolarizes, the more rapidly adjacent cells will become depolarized, leading to a more rapid regeneration and transmission of action potentials between cells. Therefore, blocking sodium channels reduces the velocity of action potential transmission within the heart reduced conduction velocity; negative dromotropy. This can serve as an important mechanism for suppressing tachycardias that are caused by abnormal conduction e.

By depressing abnormal conduction, reentry mechanisms can be interrupted. Besides affecting phase 0 of action potentials, sodium-channel blockers may also alter the action potential duration APD and effective refractory period ERP. These effects on ERP are not directly related to sodium channel blockade, but instead are related to drug actions on potassium channels involved in phase 3 repolarization of action potentials.

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The drugs in these subclasses also differ in their efficacy for reducing the slope of phase 0, with IC drugs having the greatest and IB drugs having the smallest effect on phase 0 IA drugs are intermediate in their effect on phase 0. The following summarize these differences:. Increasing or decreasing the APD and ERP can either increase or decrease arrhythmogenesis, depending on the underlying cause of the arrhythmia.

Increasing the ERP, for example, can interrupt tachycardia caused by reentry mechanisms by prolonging the duration that normal tissue is unexcitable its refractory period. This can prevent reentry currents from re-exciting the tissue. On the other hand, increasing the APD can precipitate torsades de pointesa type of ventricular tachycardia caused by afterdepolarizations. By mechanisms not understood and unrelated to blocking fast sodium channels, Class I antiarrhythmics can suppress abnormal automaticity by decreasing the slope of phase 4, which is generated by pacemaker currents.

Calcium channel blockers

The direct effect of Class IA antiarrhythmic drugs on action potentials is significantly modified by their anticholinergic actions. Inhibiting vagal activity can lead to both an increase in sinoatrial rate and atrioventricular conduction, which can offset the direct effects of the drugs on these tissues. Although a IA drug may effectively depress atrial rate during flutter, it can lead to an increase in ventricular rate because of an increase in the number of impulses conducted through the atrioventricular node anticholinergic effectthereby requiring concomitant treatment with a beta-blocker or calcium-channel blocker to slow AV nodal conduction.

These anticholinergic actions are most prominent at the sinoatrial and atrioventricular nodes because they are extensively innervated by vagal efferent nerves.

Different drugs within the IA subclass differ in their anticholinergic actions see table below. The following table summarizes Class I compounds in terms of their therapeutic use and some special or distinguishing characteristics. More detailed information on specific drugs can be found at www.Doctors, too, don't always check blood pressure. Be sure to get yours checked at every doctor appointment.

If you have high blood pressure, stick with your treatment. Studies show that about half of people treated for high blood pressure don't get it under control.

That's unfortunate—and unnecessary. In some cases, a committment to making lifestyle changes—such as eating a healthful dietlosing weightreducing salt intake, and getting regular exercise —can lower blood pressure enough so that medication may not be needed. When they don't, low-cost medicines can help. In most cases, the cause of high blood pressure is unknown.

Anyone can develop it, even if they are thin, healthy, and exercise regularly. But several factors are known to increase the risk, including:. High blood pressure is often linked to weight gain, poor diet, and sedentary lifestyle. Family history, getting older and gaining weight also play a role. A high salt diet may contribute as well. For the same reasons, and perhaps due to genetic factors as well, black Americans are more likely to have high blood pressure and to develop it at a younger age.

And studies indicate they are more sensitive than Caucasian people to the blood pressure-raising effects of salt in their diet. Your heart is a powerful muscle that pumps blood through your arteries. To withstand that pressure, healthy arteries need to be flexible. Anything that makes them less so—getting older, certain medications, and risk factors such as inactivity, obesity, and smoking, or having a genetic predisposition, for example—can make blood pressure rise.

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You should have your blood pressure checked at least once every two years, and more often if you're 50 or older or have other risk factors for hypertension. For most people, it's a good idea to have it done during every visit to a health-care provider. If your initial reading is elevated, don't panic. To improve the accuracy:. If your blood pressure is high, your doctor may take another reading after about 5 minutes or so.

If the reading is still elevated and you have no history of previous high readings, you should get another reading in a couple of weeks before initiating treatment. Good blood pressure equipment can be purchased at most drugs stores.

In fact, in such circumstances, your doctor may ask you to measure your blood pressure several times or even every day over a period of a week or so. He or she will calculate the average of all the measurements to get a final reading.

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The reason to be sure your blood pressure is indeed elevated before starting on a medication is that the medicines used to treat it can have side effects. Plus, people with normal blood pressure should not take medicines because having excessively low blood pressure can be dangerous, increasing the risk for experiencing dizziness and putting some people at risk for accidents and falls.

See our Ratings of blood pressure monitors here.

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Blood pressure is the force exerted by blood against the walls of your arteries as it flows through your body. It is measured as two numbers, one over the other—for example, over The diastolic lower number is the pressure when the heart rests between contractions.Metrics details. Since then we have continued our studies further and found that some cardioprotective drugs are NCX1 stimulators.

Sildenafil a phosphodiesterase-5 inhibitor further increased the pinacidil-induced augmentation of I NCX1. In paper, here I review the NCX stimulants that enhance NCX function among the cardioprotective agents we examined such as nicorandil, pinacidil, SNP, sildenafil and flecainide, in addition to atrial natriuretic ANP and dofetilide, which were reported by other investigators.

The major difference between them is in the orientation of the three C-terminal TMS, but not in the large intracellular loop containing about amino acids between TMS 5 and 6 [ 67 ]. The pharmacological agents for NCX1 regulation are classified into two groups: stimulators and inhibitors.

The pharmacology of NCX1 inhibitors has been reported by several researchers [ 9 — 11 ]. On the other hand, there are next to no reports on NCX1 stimulants among cardioprotective agents. This review is about the properties of NCX1 stimulators among cardioprotective drugs including nicorandil, pinacidil, flecainide, sodium nitroprusside SNPand sildenafil, which we have investigated to date, as well as atrial natriuretic peptide ANP and dofetilide.

Horie et al. Nicorandil N- 2-hydroxyethyl -nicotinamide nitrate is widely used as an anti-angina drug with nitrate-like activity and KATP channel opening activity.

Nicorandil has multiple additional effects including anti-fibrotic activity, anti-apoptotic activity, and reactive oxygen species ROS prevention [ 17 ]. In addition, nicorandil acutely increases cGMP levels by activating soluble GC via NO-dependent or -independent pathways in smooth muscles and cardiac cells [ 20 — 23 ]. Liou et al. Similar results were obtained by Minamiyama et al. Effect of nicorandil on I NCX1 modified from [ 24 ] with permission.

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We examined the effects of nicorandil on I NCX in cells expressing wild-type NCX1, its mutants, and in isolated guinea-pig cardiac ventricular myocytes [ 24 ] Fig. The enhancement ratios of I NCX1 by nicorandil were similar between the wild-type NCX1 expressing cells and the guinea-pig cardiac ventricular myocytes [ 24 ] Fig.

These results indicated that the large intracellular loop between TMS 5 and 6 may be responsible for the site of action of nicorandil on NCX1.

Pinacidil, which was initially developed as an antihypertensive drug, is a non-selective KATP channel opener without nitrate-like activity. Effect of pinacidil on I NCX1 modified from [ 27 ] with permission. On the other hand, two groups suggested a possible link between KATP channels and NO generation in the rabbit mesenteric artery and rat heart [ 3031 ].

The next question that arises is how pinacidil generates NO. We tested NO production by pinacidil using a fluorometric assay kit in single cardiomyocytes. Krenz et al. There are two reports that affirm these results.

Holmuhamedov et al. In the case of a low or high concentration of pinacidil, the signaling pathway that enhances NCX1 function may be different.

KATP channels in vascular smooth muscle cells regulate the membrane potential.Sodium-activated potassium K Na channels have been suggested to set the resting potential, to modulate slow after-hyperpolarizations, and to control bursting behavior or spike frequency adaptation Trends Neurosci Studies found that Slack channels were highly expressed in nociceptive dorsal root ganglion neurons and modulated their firing frequency J Neurosci Therefore, Slack channel openers are of significant interest as putative analgesic drugs.

We screened the library of pharmacologically active compounds with recombinant human Slack channels expressed in Chinese hamster ovary cells, by using rubidium efflux measurements with atomic absorption spectrometry.

Psychotropic drugs structurally related to loxapine were also evaluated in patch-clamp experiments, but none was found to be as active as loxapine.

Loxapine properties were confirmed at the single-channel level with recombinant rat Slack channels. In dorsal root ganglion neurons, loxapine was found to behave as an opener of native K Na channels and to increase the rheobase of action potential. This study identifies new K Na channel pharmacological tools, which will be useful for further Slack channel investigations.

Abstract Sodium-activated potassium K Na channels have been suggested to set the resting potential, to modulate slow after-hyperpolarizations, and to control bursting behavior or spike frequency adaptation Trends NeurosciSodium nitroprusside SNPsold under the brand name Nitropress among others, is a medication used to lower blood pressure.

Common side effects include low blood pressure and cyanide toxicity. Sodium nitroprusside was discovered as early as and found to be useful in medicine in Sodium nitroprusside is intravenously infused in cases of acute hypertensive crises.

Nitric oxide reduces both total peripheral resistance and venous return, thus decreasing both preload and afterload. So, it can be used in severe congestive heart failure where this combination of effects can act to increase cardiac output. In situations where cardiac output is normal, the effect is to reduce blood pressure. This compound has also been used as a treatment for aortic valve stenosis[12] oesophageal varices[13] myocardial infarction[14] pulmonary hypertension[15] [16] [17] respiratory distress syndrome in the newborn[18] [19] shock, [19] and ergot toxicity.

Adverse effects by incidence and severity [8] [10] [21]. Sodium nitroprusside should not be used for compensatory hypertension e.

It should not be used in patients with vitamin B 12 deficiency, anaemia, severe renal disease, or hypovolaemia. Its use in pregnant women is advised against, although the available evidence suggests it may be safe, provided maternal pH and cyanide levels are closely monitored. The only known drug interactions are pharmacodynamic in nature, that is it is possible for other antihypertensive drugs to reduce the threshold for dangerous hypotensive effects to be seen.

Due to its cyanogenic nature, overdose may be particularly dangerous. Treatment of sodium nitroprusside overdose includes the following: [10] [24]. Haemodialysis is ineffective for removing cyanide from the body but it can be used to remove most of the thiocyanate produced from the above procedure. The cyanide can be detoxified by reaction with a sulfur -donor such as thiosulfatecatalysed by the enzyme rhodanese.

As a result of its breakdown to nitric oxide NOsodium nitroprusside has potent vasodilating effects on arterioles and venules veins more than arteries but this selectivity is much less marked than that of nitroglycerin. Sodium nitroprusside breaks down in circulation to release nitric oxide NO. The end result is vascular smooth muscle relaxation, which allow vessels to dilate. A role for NO in various common psychiatric disorders including schizophrenia[30] [31] [32] [33] bipolar disorder [34] [35] [36] and major depressive disorder [37] [38] [39] has been proposed and supported by several clinical findings.

These findings may also implicate the potential of drugs that alter NO signalling such as SNP in their treatment. The anion possesses idealized C 4v symmetry. Nitric oxide is a non-innocent ligand. The iron center has a diamagnetic low-spin d 6 electron configuration, although a paramagnetic long-lived metastable state has been observed by EPR spectroscopy.

The chemical reactions of sodium nitroprusside are mainly associated with the NO ligand. The former was first prepared by treating nitroprusside with sulfur. It decomposes in aqueous acid to liberate hydrocyanic acid HCN.

It breaks down rapidly upon exposure to light, although the details are poorly understood.

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It degrades when heated e. Sodium nitroprusside can be synthesized by digesting a solution of potassium ferrocyanide in water with nitric acidfollowed by neutralization with sodium carbonate : [49]. Alternatively, ferrocyanide may be oxidized with nitrite as well: [43].

For this application, sodium nitroprusside can be reversibly promoted to a metastable excited state by blue-green light, and de-excited by heat or red light. In physiology research, sodium nitroprusside is frequently used to test endothelium-independent vasodilation. Iontophoresisfor example, allows local administration of the drug, preventing the systemic effects listed above but still inducing local microvascular vasodilation. Sodium nitroprusside is also used in microbiology, where it has been linked with the dispersal of Pseudomonas aeruginosa biofilms by acting as a nitric oxide donor.

Sodium nitroprusside is also used as an analytical reagent under the name sodium nitroferricyanide for the detection of methyl ketones, amines, and thiols.

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