Reversible inhibition of acetylcholinesterase reduces breakdown of ACh at cholinergic nerve endings, so potentiating neurotransmission. Binds only to the anionic site in esterase. Mainly electrostatic and reverses readily.
Binds reversibly to α-receptors and blocks noradrenaline action.
Possesses a guanidinium group, and blocks sodium channels from the outside (non-use-dependent).
Binds to neurexins and causes massive release of ACh.
Selective for β2-receptors. Used experimentally.
Not well established. One proposal is that lithium interferes with membrane ion transport, perhaps including neuotransmitter reuptake. Actions on phosphatidyl inositol metabolism or on glycogen synthase kinase are other possible mechanisms.
Bay K 8644
Dihydropyridine. Favours Mode 2 of L-type calcium channel opening (very long openings). Highly lipid soluble and gains access to the channel via the lipid phase of the membrane.
Targets synaptobrevin. Is transported retrogradely to the cell body, and is then transferred to an inhibitory interneuron which is then unable to release its transmitter and so the motor neuron becomes more excitable.
May prove useful for controlling neoplastic growth - receptor tyrosine kinases regulate cell proliferation and differentiation.
Blocks release of NA. Taken up into nerve by uptake 1, competing with NA, and can therefore potentiate exogenously applied NA. In large does, acts as indirectly-acting sympathomimetic amines.
Synergises with antiparksonian effects of carbidopa/levodopa and potentiates actions of catecholamines. Reversible inhibition of COMT in the periphery reduces levodopa breakdown allowingmore of levodopa dose to penetrate brain.
Non-selective cholinergic antagonist (like ACh)
Unable to cross the BBB, so results in peripheral sympathomimetic effects
Can only reverse irreversible anticholinesterase activity if given within a few hours of inhibition, before the enzyme/inhibitor complex undergoes ageing.
Given in conjunction with levodopa to treat Parkinsonism. Carbidopa can't cross BBB, only effects periphery. Carbidopa inhibits levodopa decarboxylation outside the brain, allowing use of smaller doses of levodopa and reducing peripheral side effects of dopamine
Used to lower blood pressure and to ease angina. Inhibits voltage-gated calcium channels and reduces the contractile process. Grapefruit juice increases the effects.
Long-lasting vascular dilatation. Activates sodium channels which hyperpolarises the membrane which inhibits voltage-dependent calcium channels, thus reducing contraction.
Activates G-protein-coupled adenosine receptors. Action on A1 receptors is due to inhibition of calcium channel opening and increased potassium channel opening. Negative chronotropic antion on SA node and slowed AV conduction.
Also has parasympathomimetic actions. Action in glaucoma is due to reaction with M3 receptors which couple to Gq to increase cellular IP3 and DAG concentrations. Constriction of pupil aids drainage of aqueous humour and lowers intraocular pressure. Very few unwanted effects as very limited systemic absorption of topically applied drug.
Cardiac stimulant: it increases contractility and thus CO. Less effect on heart rate. ACts mainly on β1-receptors causing G-protein-mediated increase of cAMP which increases calcium influx in the cardiac myoctes. Minimal effect on β2-receptors. Can cause dysrhythmias
Produces NO, and produces vasodilatation and smooth muscle relaxation through increase of soluble guanylyl cyclase and therefore increased cGMP.
Blocks calcium channels in both cardiac and smooth muscle so has both negative inotropic and smooth muscle relaxant actions. Blocks L-type, voltage-gated calcium channels which are important in the AP plateau and in particular effects AP propagation in the SA and AV nodes. Use-dependent so is more active in tachyarhythmias. Decreases automaticity and slows AV conduction. Can cause side effects due to smooth muscle relaxation, and bradycardia.
Produces NO, and produces vasodilatation and smooth muscle relaxation through increase of soluble guanylyl cyclase and therefore increased cGMP.
Prevents propagation of nerve APs. Blocks small-diameter pain fibres at lower concentration than large fibres. pKa=2.5, much weaker base than most LAs and is mainly unionised in the body. Non-use-dependant and can gain access to the sodium channel via the lipid membrane.
Increases insulin release from functioning B-cells, thus producing the effects of insulin. Interaction with the sulphonylurea receptor, a subunit of the Katp channel in the cell membrane of B cells, causes the potassium channel to close. This cuases the cell to depolarise and activates voltage-dependent calcium channels. Calcium entry stimulates exocytosis of insulin.
Blocks the uptake of choline into the nerve cell by blocking the choline transporter.
Blocks post-synaptic ACh release. Acts through phospholipase A2 activity. Localises to the membrane via potassium channel binding moiety.
Also antianginal and antihypertensive. Blocks calcium channels in both cardiac and smooth muscle so has both negative inotopic and smooth muscle relaxant actions. Blocks L-type, voltage gated calcium channels which are important in the AP plateau and in particular affects AP propagation in the SA and AV nodes. SHows use-dependence so more active in tachycardias. Decreases automaticity and slows AV conduction.
Suppresses development of ovarian follicle by inhibiting FSH release from anterior pituitary.
Causes release of calcium from the sarcoplasmic reticulum by activating α1 receptors which initiate the PIP2 to IP3 pathway, causing calcium influx and calcium-induced calcium release. Increased calcium activates the contractile mechanism.
Irreversible inhibition of anticholinesterase potentiates actions of released ACh at cholinergic nerve-endings. Binds to enzyme's esteratic site causing irreversible phosphorylation. Causes increased peristalsis, increased secretions, bradycardia, bronchoconstriction, decreased intraocular pressure. Fasciculation and increased twitch tension at NMJ.
Inhibits gonadal function by suppressing mid-cycle surge of gonadotrophins. Acts on hypothalamus and anterior pituitary (GnRH and GnRHR).
Mimics the effect of ACh on muscarinic receptors. Non-selective to subtype.
Partial agonist of progesterone receptors, it sensitises the uterus to prostaglandins (given in conjunction with prostaglandins as a medical alternative to surgical termination of pregnancy). Possibly has antiretroviral properties.
Selective for α2-receptors. Used in veterinary medicine for its sedative effects through an action on α2-receptors in the CNS.
Various botulinium toxins target synaptobrevin, SNAP-25 or syntaxin to cleave the target SNARE.
Binds tightly to the amine binding site of the VMAT-2 vesicular monoamine transporter. Also leads to long-lasting depletion of stored NA and 5-HT in the brain.
Prevents propagation of nerve APs. Blocks small-diameter pain fibres and lower concentration that large fibres. Use-dependent block of voltage gated sodium channels from inside cell membrane. Penetrates cell membrane in its lipid-soluble, uncharged form. Less active in inflamed tissue, where lower pH increases ionisation of the weakly basic local anaesthetic. Ester-type LAs are generally shorter acting that lidocaine etc, but more likely to cause allergic reaction.
Irreversibly alkylates the muscarinic receptor.
Reduces release of noradrenaline and lowers blood pressure. Acts mainly in the CNS, where it is taken up into adrenergic neurones and converted into false transmitter methylnoradrenaline. This is released and acts on α2 adrenoceptors decreasing the release of NA.
Reversible inhibition of acetylcholinesterase reduces breakdown of ACh at cholinergic nerve-endings, so potentiating transmitter action. Binds to both esteratic and anionic sites in the enzyme. The esterase is carbamylated.
Similar method of action to hexamethonium
Potent and irreversible inhibitor of iNOS in activated macrophages.
Experimental use. Binds with greater specificity to muscarinic receptors.
Opens Katp channels. Leads to smooth muscle relaxation.
Non-selective reversible inhibitor of MAO used in the treatment of refractory depression.
Selectively antagonises M! muscarinic receptors.
Action most prominent after prolonged wakefulness. Non-selective and also inhibits phosphodiesterase, the enzyme that breaks down cyclic nucleotides eg cAMP
A quaternary lidocaine derivative, permanantly charged and lipophobic. A powerful blocker of volatage-sensitive sodium conductance when applied intracellularly.
Acts on the distal renal tubule to increase sodium reabsorption and increase excretion of potassium and hydrogen ions. Mineralocorticoid interact with intracellular receptors in the kidney controlling transcription of specific genes (COX-2, interleukins and cytokines) that increase the number of sodium channels and pumps.
Inhibits platelet aggregation. Has vasodilator activity; prevents platelet adenosine uptake and cyclic GMP phosphodiesterase action.
Increases insulin release from functioning B cells, thus producing the effects of insulin. Interaction with the sulphonylurea receptor, which is a subunit of the Katp channel in the cell membrane of B cells, causes the potassium channel to close. This causes the cell to depolarise and activates voltage-dependent calcium channels. Calcium entry stimulates exocytosis of insulin.
Closely related to NA, and has adrenergic and dopaminergic effects
Paralysis of skeletal muscle. Reversible competitive antagonism at muscle-type nicotinic receptors. Inhibits binding of ACh to receptors at the muscle end-plate. EPP fails to reach treshold for initiation and propagation of the AP along the muscle fibre. Action reversed by anticholinesterases.
Blocks transmission by causing prolonged depolarisation.
Blocks action of endogenous and exogenous agonists on α1-receptors.
Used in treatment of alcohol addiction, can be used experimentally to inhibit DBH. May act by chelating the copper ion which is essential for enzyme function.
Especially ganglion type nicotinic receptors and one CNS receptor. It acts as a CNS stimulant and activates the sympathetic system.
Competitive inhibitor of TOH and used experimentally to reduce NA production.
Selective for α2-receptors. Used experimentally.
Prevents propagation of nerve APs. Blocks small-diameter pain fibres at lower conc than large.Blocks open and inactivated sodium channels, and shows use-dependence, so more likely to act in damaged, depolarised tissue. Less active in inflamed tissue, where lower pH increases ionisation of the weakly basic LA. Sodium channel block reduces rate of phase 0 depolarisation, increasing effective refractory period and slowing AV conduction.
Tubocurarine is a long-duration non-depolarising neuromuscular blocking agent that is a competitive inhibitor of nicotinic neuromuscular acetylcholine receptors. It is a type of curare. It also acts as a ganglion blocker, sometimes resulting in hypotension, and causes histamine release.
Blocks open and inactivated sodium channels in the cell membrane ('use-dependent') to reduce rate of phase 0 depolarisation thus causing an increase in the effective refractory period and slowed AV conduction. Laso produces some slowing of AP repolarisation (Class III action).
Selectively inhibits NOS in neurons. Does not affect eNOS or iNOS.
Selectively breaks down cyclic GMP and used to treat impotence.
Cholera toxin acts on Gs, and catalyses a conjugation reaction (ADP ribosylation) on the alpha subunit. It causes persistant activation, leading to uncontrolled adenylyl cyclase activation and symptoms such as excessive secretion of fluid from the GI epithelium.
Binds covalently and irreversibly to α receptors and blocks noradrenaline action. Can cause postural hypotension and tachycardia.
Inhibits sodium reabsorption in the distal nephron. Has limited diuretic efficacy. Reduces potassium excretion. Can be used as an antihypertensive. It is a competetive antagonist of aldosterone and causes diuresis by preventing production of the aldosterone mediator that normally causes influx of sodium by activating the sodium channel in the luminal membrane of the collecting tubule.
Slightly selective for α2-receptors, can be used as antihypertensive, but missing a single dose can result in rebound hypertension.
Use-dependent block of voltage-gated sodium channels from inside cell membrane. Penetrates cell membrane in its lipid soluble, uncharged form. Less active in inflamed tissue, where the lower pH increases ionisation of the weakly basic LA. Also inhibits action of monoamine transporters, leading to increased NA effects.
Parasympathetic actions: contracts smooth muscle(gut, bladder, pupil), decreases rate and force of heartbeat, glandular secretion, inhibits neurotransmitter release.
Relief during asthma attacks. Selective for β2.
Was used in asthma to relax bronchi through action on β2-receptors but the increase in heart rate from β1-receptor stimulation was a major problem.
Selective for the nicotinic receptor at the NMJ. Block transmission by causing prolonged depolarisation. The only depolarising blocker in clinical use.
Selectively inhibits MAO-B, used in treatment of Parkinson's. Maintains levels of NA.
Shows high affinity for α2-receptors, and moderate affinity for α1-receptors, some 5-HT receptors and some dopamine receptors.
A catecholamine that is also an adrenoceptor agonist with greater specificity for β-adrenoceptors than α.
Mainly mediated by 5-HT receptors, partial α agonist.
Selectively inhibits MAO-A, used in depression. Maintains levels of NA.
Blocks of action of endogenous and exogenous agonists on β-receptors. Blocks sympathetic drive, reducing pacemaker activity and increasing AV conduction time. Reduces the slow inward calcium current which affects phase 2 of the AP. Has additional class 1 action.
Paralyses skeletal muscle. Reversible competitive antagonism at muscle-type nicotinic receptors. Inhibits binding of ACh to the receptors at the muscle end-plate. EPP fails to reach threshold for initiation and propagation of the AP along the muscle fibre. Action reversed by anticholinesterases.
Conventional Competitive antagonist of ganglionic nicotinic receptor.
Prevents ovulation by inhibiting LH release.
Causes ADP-ribosylation of αi subunit of Gi and prevents activation of Gi in response to receptor stimulation.
Used in chronic asthma. Inhibits clonal proliferation of T&B cells and macrophage activation. Reduction in chronic inflammation and in autoimmune and hypersensitivity reactions. Interacts with intracellular receptors for various cytokines esp IL-2
Inhibition of neuronal reuptake of monoamine, inhibition of monoamine oxidase, inhibition of the vesicular monoamine transporter. Raised cytosolic levels of monoamines and release from nerve terminals, mainly by reverse operation of the monoamine transporter. Increased monoamine levels in synapse. Sympathomimetic action due to release of noradrenaline in the periphery - adrenoceptor stimulation.
Non-selective for different forms of NOS. D-isomer is inactive.
Insecticide to kill lice. Irreversibly binds (covalently).
Has powerful vasodilator effects caused by activation of Katp channels implicaed in the control of membrane potential in vascular smooth muscle and in insulin secretion (it markedly increases blood sugar).
Blcoks action of endogenous and exogenous agonists on β1-receptors. Reduces BP in hypertensive patients, and slows heart rate in angina.
Blocks uptake of NA by NET protein via uptake 1, and blocks uptake of serotonin by uptake 1.
Non-competitively and reversibly blocks the transporter which carries ACh into storage vesicles.
Competitive reversible antagonism at all muscarinic receptors. Inhibits secretions. Tachycardia. Relaxes smooth muscle. Antiemetic.
Competes with endogenous oestrogen for the oestrogen receptor, preventing cell activation and proliferation. Clinically used against breast cancer.
Use-dependent blockade of ganglionic transmission which is interpreted as a block of the open channel. Causes both loss of sympathetic control and parasympathetic responses.
Four isomers, each of which has different actions. R,R: β-blocker, weak α1-blocker. R,S: no activity. S,R: α1-blocker, very weak β-blocker. S,S: α1-blocker.
Inhibits reuptake of NA into noradrenergic neurones and 5-HT into serotonergic neurons, so potentiating transmitter action. The clinical effects aren't seen for a few weeks, meaning that longer term changes are required. Amitryptyline also reduces neuropathic pain, acting as an analgesic due to inhibition of the opening of neuronal voltage-gated sodium channels.
You're not logged in!
Compare scores with friends on all Sporcle quizzes.