It is the immediate precursor of dopamine & is able to penetrate the blood-brain barrier to replenish the dopamine content of the corpus striatum. It is decarboxylated to dopamine in the brain by dopa decarboxylase, & is has beneficial effects produced through the actions of dopamine on D2 receptors. Dopamine itself is not used, owing to its inability to cross the blood-brain barrier
Dopamine agonists selective for the D2 receptor
Facilitation of neuronal dopamine release & inhibition of its reuptake into nerves, & additional muscarinic blocking actions
It selectively inhibits the MAOB enzyme in the brain that is normally responsible for the degradation of dopamine. By reducing the catabolism of dopamine, the actions of L-dopa are potentiated, thus allowing the dose to be reduced by up to 1/3. There is evidence to suggest it may slow the progression of the underlying neuronal degeneration in Parkinson's disease
Dopamine is broken down by a 2nd pathway, in addition to that of MAOB. The enzyme COMT is responsible for the degradation of dopamine to inactive methylated metabolites. COMT inhibitors specifically inhibit this enzyme
Antagonists at the muscarinic receptors that mediate striatal cholinergic excitation. It's major action in the treatment of Parkinson's disease is to reduce the excessive striatal cholinergic activity that characterises the disease
The aim of using beta-adrenoceptor antagonists in cardiac disease is to block beta-adrenoceptors in the heart. This has the effect of causing a fall in HR (slowing of phase 4), in systolic blood pressure, in cardiac contractile activity & in myocardial oxygen demand
Block L-type calcium channels found in the heart & in the vascular smooth muscle, thereby reducing calcium entry into cardiac & vascular cells. This decrease in intracullular calcium reduces cardiac contractility & causes vasodilation, which results in several effects: reduced preload due to the reduced venous pressure; reduced afterload due to the reduced arteriolar pressure; increased coronary blood flow; reduced cardiac contractility & thus reduced myocardial O2 consumption; & a decreased HR. High doses of these drugs affect AV nodal conduction
Short-acting. Block L-type calcium channels in vascular cells. They do not affect cardiac contractility, or AVN conduction, & the beneficial effects are due to increased coronary flow & peripheral vasodilation
Block voltage-dependent sodium channels in their open (activated) or refractory (inactivated) state. Their effects are to slow phase 0 (increasing the effective refractory period) & phase 4 (reducing automatically), & to prolong action potential duration
Blocking voltage-dependent sodium channels in their refractory (inactivated) state, i.e. when depolarised, as occurs in ischaemia. Binding to open channels during phase 0, & dissociating by the next beat, if the rhythm is normal, but abolishing premature beats
Blocks sodium channels, but shows no preference for refractory channels. Therefore resulting in a general reduction in the excitability of the myocardium
Potassium-channel blockers. They prolong cardiac action potential duration (increased QT interval on the ECG), & prolong the effective refractory period
Acts at A1 receptors in cardiac conducting tissue & causes myocytes hyperpolarisation. This acts to slow the rise of an action potential & brings about delay in conduction
Block the reduction of vit K epoxide, which is necessary for its action as a co-factor in the synthesis of factors II, VII, IX & X
Activates antithrombin III, which limits blood clotting by inactivating thrombin & factor X. It also inhibits platelet aggregation, possibly as a result of inhibiting thrombin.
Blocks the synthesis of thromboxane A2 from arachidonic acid in platelets by acetylating & thus inhibiting the enzyme cyclooxygenase. Thromboxane A2 stimulates phospholipase C, thus increasing calcium levels & causing platelet aggregation. It also blocks the synthesis of prostacyclin from endothelial cells, which inhibits platelet aggregation. However this effect is short lived because endothelial cells, unlike platelets, can synthesise new cyclooxygenase
Causes inhibition of the phosphodiesterase enzyme that hydrolyses cAMP. Increased cAMP levels result in decreased calcium levels & inhibition of platelet aggregation
Inhibits activation of the glycoprotein IIb/IIIa receptor on the surface of platelets, which is required for aggregation to occur
Is an antibody fragment directed towards the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor of platelets. Binding & inactivation of the GPIIb/IIIa receptor prevents platelet aggregation
Airway smooth muscle does not have a sympathetic nervous supply, but it does contain beta2-adrenoceptors that responds to circulating adrenaline. The stimulation of beta2-adrenocreptors leads to a rise in intracellular cAMP levels & subsequent smooth muscle relaxation & bronchodilation
Parasympathetic vagal fibres provide a bronchoconstrictor tone to the smooth muscle of the airways. They are activated by reflex on stimulation of sensory (irritant) receptors in the airway walls. Muscarinic antagonists act by clocking muscarinic receptors, especially the M3 subtype, which responds to this parasympathetic bronchoconstrictor tone
Increases cAMP levels in the bronchial smooth muscle cells by inhibiting phosphodiesterase, an enzyme which catalyses the hydrolysis of cAMP to AMP. Increases cAMP relaxes smooth muscle, causing bronchoconstriction
Believed to act at leukotriene receptors in the bronchiolar muscle, antagonising endogenous leukotrienes, thus causing bronchodilation. They are thought to be partly responsible for airway narrowing which is sometimes observed with the use of NSAIDs in asthmatic people. The NSAIDs inhibits cyclooxygenase, & divert arachidonic acid breakdown via the lipoxygenase pathway, liberating leukotrienes among other mediators
These drugs appear to stabilise antigen-sensitised mast cells by reducing calcium influx & subsequent release of inflammatory mediators
Depress the inflammatory response in brinchial mucosa & so diminish bronchial hyperresponsiveness. The specific effects include: reduced mucosal oedema & mucus production, decreased local generation of prostaglandins & leukotrienes, with less inflammatory-cell activation, adrenoceptor up-regulation, long-term reduced T-cell cytokine production, & reduced eosinophil & mast-cell infiltration of bronchial mucosa
Blocking voltage-dependent sodium channels in their refractory (inactivated) state, i.e. when depolarised, as occurs in ischaemia, • Binding to open channels during phase 0, & dissociating by the next beat, if the rhythm is normal, but abolishing premature beats, • Decreasing action potential duration, increasing the effective refractory period
2 mechanisms of action: use-dependent block of voltage-gated sodium channels; it also increases the GABA content of the brain when given over a prolonged period
Inhibition of low-threshold calcium currents
Irreversible inhibition of GABA transaminase
Acts via an effect on sodium channels, & inhibiting the release of excitatory amino acids
Lipophile drug that was designed to act like GABA in the CNS (agonist), though it does not appear to have GABA-mimetic actions. Its mechanism of action remains elusive, but its antiepileptic action almost certainly involved voltage-gated calcium-channel blockade
Cause potentiation of chloride currents through the GABAA/CL-c channel complex
These drugs block sodium reabsorption by the principal cells, thus reducing the potential difference across the cell & reducing K+ secretion. Secretion of H+ from the intercalated cells is also decreased
Act by inhibiting the membrane Na+/K+ ATPase pu,p. This increases incracellular Na+ concentration, thus reducing the Na+ gradient across the membrane & decreasing the amount of calcium pumped out the cell by the Na+/Ca2+ exchanger during diastole. Consequently, the intracellular calcium concentrations rises, thus increasing the force of cardiac contraction & maintaining normal BP. At therepeutic doses they indirectly decrease the HR, slow AV conductance & shorten the atrial action potential by simulating vagal activity. The direct effects are mainly due to loss of intracellular potassium, & are most pronounced at high doses
The type III PDE isoenzyme is found in myocardial & vascular smooth muscle. Phosphodiesterase is responsible for the degradation of cAMP; thus, inhibiting this enzyme raises cAMP levels & causes an increase in myocardial contractility & casodilation. Cardia coutput is increassed, & pulmonary wedge pressure & total peripheral resistance are reduced, without much change in HR or BP
Precursor of noradrenaline. It activates dopamine receptors & alpha & beta-adrenoceptors. When administered by IV infusion, dopamine acts on: dopamine receptors, causing vasodilation in the kidneys at low doses; alpha1-adrenoceptors, causing vasoconstriction in other vasculature; beta1-adrenoceptors, causing positive inotropic & chronotropic effects
Inhibit the Na+/K+/2Cl- co-transporter in the luminal membrane. This increases the amount of sodium reaching the collecting duct & thereby increases K+ & H+ secretion. Calcium & magnesium reabsorption is also inhibited, owing to the decrease in potential difference across the cell normally generated from the recycling of potassium. They also have a venodilator action, which often brings about relief of clinical symptoms prior to the onset of diuresis
Inhibit the Na+/Cl- co-transporter in the luminal membrane. They increase the secretion of K+ & H+ into the collecting ducts but they decrease Ca2+ excretion by a mechanism possibly involving the stimulation of a Na+Ca2+ exchanhe across the basolateral membrane; this is due to reduced tubular cell sodium concentration
Competitive antagonist at aldosterone receptors & thus reduces Na+ reabsoption & therefore K+ & H+ secretion. The degree of diuresis depends on aldosterone levels
Freely filtered at the glomerulus, but only partially, if at all, reabsorbed. Passive water reabsorption is reduced by the presence of this non-reabsorbable solute within the tubule lumen. The net effect is increased water loss, with a relatively smaller loss of sodium
Inhibition of ACE with consequent reduced angiotensin II & aldosterone levels & increased bradykinin levels. This therefore causes vasodilation with a consequent reduction in peripheral resistance, little change in HR & cardiac output & reduced sodium retention
Most nitrates are prodrugs, decomposing to form nitric oxide (NO), which activates guanylyl cyclase, thereby increasing the levels of cyclic guanosine monophosphate (cGMP). Protein kinase G is activated & contractile proteins are phosphorylated. Dilatation of the systemic veins decreases preload & thus the oxygen demand of the heart, while dilatation of the coronary arteries increases blood flow & oxygen delivery to the myocardium
Appears to interfere with the action of inositol triphosphate in vascular smooth muscle, thereby reducing peripheral resistance & BP
Cause inhibition at the angiotensin-II receptor, resulting in vasodilation with a consequent reduction in peripheral resistance
cause inhibition of alpha1-adrenoceptor-mediated vasoconstriction – thus reducing peripheral resistance & venous pressure. They also lower plasma LDL, cholesterol levels, VLDL, T levels, thus reducing the risk of CAD
activates vascular smooth muscle ATP-sensitive potassium channels, resulting in hyperpolarisation of the cell membrane & consequent reduced calcium entry through L-type channels. The overall effect is inhibition of smooth muscle contraction, & subsequent vasodilation
A prodrug that spontaneously decomposes into NO inside smooth muscle cells. NO activates guanylyl cyclase, thus increasing intracellular cGMP levels, & causing vasodilation
Alpha2-adrenoceptor agonist. The activation of presynaptic alpha2-adrenoceptors causes inhibition of noradrenaline release & consequent vasodilation. The activation of postsynaptic alpha2-adrenoceptors causes vasoconstriction, although presynaptic effects dominate. They reduce the activity of the vasomotor centre in the brain, causing reduced sympathetic activity & subsequent vasodilation. They also reduce HR & cardiac output
Reversibly inhibit the enzyme HMC CoA reductase, which catalyses the rate-limiting step in the synthesis of cholesterol: HMG CoA becomes mevalonic acid which becomes cholesterol. The decrease in cholesterol synthesis also increases the number of LDL receptors, thus decreasing LDL levels
Several different mechanisms: stimulation of lipoprotein lipase, thus reducing the triglyceride content of VLDLs & chylomicrons; stimulation of hepatic LDL clearance, by increasing hepatic LDL uptake; reduction of plasma triglyceride, LDL, & VLDL concentrations; & increase of HDL-cholesterol concentration (except bezafibrate). Gemfibrozil decreases lipolysis & may decrease VLDL secretion
It has the following effects: it inhibits cholesterol synthesis, thereby decreasing VLDL & thus LDL production; it stimulates lipoprotein lipase, thus reducing the chylomicrons; it increases HDL-cholesterol; it increases the level of tissue plasminogen activator; & decreases the levels of plasma fibrinogen
Basic anion exchange resins act by binding bile acids in the intestine, thus preventing their reabsorption & promoting hepatic conversion of cholesterol into bile acids. This increases hepatic LDL receptor activity, thus increasing the breakdown of LDL-cholesterol. Plasma LDL-cholesterol is therefore lowered
Mimics endogenous glucose & is utilised by cells
Acts on the liver to convert glycogen to glucose, & to synthesise glucose from non-carbohydrate precursors (gluconeogenesis). The overall effect is to raise plasma glucose levels
Mimic endogenous insulin
Block ATP-dependent potassium channels in the membrane of the pancreatic beta-cells, causing depolarisation, calcium influx & insulin release
Increases the pripheral utilisation of glucose, by increasing uptake, & decreasing gluconeogenesis. To work, it requires the presence of endogenous insulin,; thus, patients must have some functioning beta-cells
It inhibits intestinal alpha-glucosidases, & delays the absorption of starch & sucrose
Believed to reduce peripheral insulin resistance, leading to a reduction in plasma glucose
Cause irreversible inhibition of H+/K+ ATPase that is responsible for H+ secretion from parietal cells. They are inactive prodrugs & are converted at acidic pH to sulphonamide, which combines covalently & thus irreversibly with -SH groups on H+/K+ ATPase. This inhibition is highly specific & localised
Competitively block the action of histamine on the parietal cell by their antagonism of H2 receptors
A synthetic analogue of prostaglandin E. It imitates the action of endogenous prostaglandins (PGE2 & PGI2) in maintaining the integrity of the gastroduodenal mucosal barrier, & promotes healing
Consist of alkaline Al3+ & Mg2+ salts that are used to raise the luminal pH of the stomach. They netralise acid &, as a result, may reduce the damaging effects of pepsin, which is pH dependent. Additionally, AL3+ &Mg2+ salts bind & inactivate pepsin
Agonist action at opioid receptors
Inhibition of the enzyme cyclooxygenase. This enzyme is involved in the metabolism of arachidonic acid to form the prostanoids, i.e. that 'classic prostaglandins', prostacyclin & thromboxane A2. This acts as a competitive substrate
Inhibition of the enzyme cyclooxygenase. This enzyme is involved in the metabolism of arachidonic acid to form the prostanoids, i.e. that 'classic prostaglandins', prostacyclin & thromboxane A2. This causes acetylation of the active site
Short-acting (half-life 2-4h). Act by specific antagonism at opioid receptors: μ, δ & ĸ receptors are blocked more or less equally. They block the actions of endogenous opioids well as of morphine-like drugs
Long-acting. Block L-type calcium channels in vascular cells. They do not affect cardiac contractility, or AVN conduction, & the beneficial effects are due to increased coronary flow & peripheral vasodilation
Long-acting (half-life 10h). Act by specific antagonism at opioid receptors: μ, δ & ĸ receptors are blocked more or less equally. They block the actions of endogenous opioids as well as of morphine-like drugs
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