The mechanism of action of first-generation neuroleptics (haloperidol)

Neuroleptic, or antipsychotic, agents are a group of drugs used to treat schizophrenia and other types of psychoses. Haloperidol an older typical, or first-generation, neuroleptic is non-selective and binds to a broad range of receptors. It can bind to dopamine D1 and D2, 5-HT2, histamine H1 and 2 adrenergic receptors in the brain. The efficacy of neuroleptics is thought to be due to antagonism of dopamine receptors in the mesolimbic and mesofrontal systems. The adverse effects of typical neuroleptics include tachycardia, impotence and dizziness, and these unwanted effects are caused by non-selective interaction at the adrenoreceptor. Other adverse effects include and sedation and weight gain, which is due to histamine H1 receptor blockade.

MECHANISM OF ACTION furosemide The diuretics are generally divided into four major classes, which are distinguished by the site at which they impair sodium reabsorption [1,2]:

Loop diuretics act in the thick ascending limb of the loop of Henle Thiazide-type diuretics in the distal tubule and connecting segment (and perhaps the early cortical collecting tubule) Potassium-sparing diuretics in the aldosterone-sensitive principal cells in the cortical collecting tubule Acetazolamide and mannitol act at least in part in the proximal tubule

To appreciate how diuretics act, it is first necessary to review the general mechanism by which sodium is reabsorbed. Each of the sodium-transporting cells contains Na-KATPase pumps in the basolateral membrane [3]. These pumps perform two major functions: they return reabsorbed sodium to the systemic circulation; and they maintain the cell sodium concentration at relatively low levels. The latter effect is particularly important since it allows filtered sodium to enter the cells down a favorable concentration gradient via carrier-mediated transport.

Mechanism of action mefenamic acid

Mefenamic acid is a competitive inhibitor of COX-1 and COX-2, which are responsible for the first committed step in prostaglandin biosynthesis.[3]Decreasing the activity of these enzymes thus reduces the production of prostaglandins, which are implicated in inflammation and pain processes.[4

Mechanism of action of dapsone

As an antibacterial, dapsone inhibits bacterial synthesis of dihydrofolic acid, via competition with para-aminobenzoate for the active site of dihydropteroate synthetase.[9] Though structurally distinct from dapsone, the sulfonamide group of antibacterial drugs also work in this way. When used for the treatment of skin conditions in which bacteria do not have a role, the mechanism or action of dapsone is not well understood. Dapsone has anti-inflammatory and immunomodulatory effects,[10] which are thought to come from the drug's blockade of myeloperoxidase. This is thought to be its mechanism of action in treating dermatitis herpetiformis.[11] As part of the respiratory burst that neutrophils use to kill bacteria, myeloperoxidase converts hydrogen peroxide (H2O2) into hypochlorous acid (HOCl). HOCl is the most potent oxidant generated by neutrophils, and can cause significant tissue damage during inflammation. Dapsone arrests myeloperoxidase in an inactive intermediate form, reversibly inhibiting the enzyme. This prevents accumulation of hypochlorous acid, and reduces tissue damage during inflammation.[12][13][14][15][16] Myeloperoxidase inhibition has also been suggested as a neuron-sparing mechanism for reducing inflammation in neurodegenerative diseases such asAlzheimer's disease and stroke.[17] Though dapsone is an anti-inflammatory agent and not a steroid, it does not fit the usual definition of an NSAID. By definition, NSAIDs block cyclo-oxygenase as their primary mechanism of action, which dapsone does not do.

Mechanism of Action of reserpine

Reserpine irreversibly blocks the vesicular monoamine transporter (VMAT). This normally transports free intracellularnorepinephrine, serotonin, and dopamine in the presynaptic nerve terminal into presynaptic vesicles for subsequent release into the synaptic cleft ("exocytosis"). Unprotected neurotransmitters are metabolized by MAO (as well as by COMT) in the cytoplasm and consequently never excite the post-synaptic cell. It may take the body days to weeks to replenish the depleted VMAT, so reserpine's effects are longlasting. As the result of above, reserpine can cause drug-induced Parkinson's Disease.
[5] [4]

Mechanism of Action flurazepam EFFECTS OF FLURAZEPAM ON EEG DIFFER FROM THOSE OF BARBITURATES IN THAT FAST ACTIVITY SEEMS TO BE INCREASED ONLY IN FRONTAL LOBE & DOES NOT SPREAD TO OCCIPITAL LOBE. IN DOSES UP TO 30 MG IT NEITHER AFFECTS REM SLEEP NOR CAUSES A REBOUND AFTER WITHDRAWAL, BUT DOSES OF 60 MG SUPPRESS REM SLEEP WITHOUT REBOUND. FLURAZEPAM DECREASES SLEEP

LATENCY, TIME IN STAGE 4, & WAKE TIME, & INCREASES TOTAL SLEEP TIME FOR AS LONG AS 22 NIGHTS OF USE. /FLURAZEPAM DIHYDROCHLORIDE/

Mechanism of action of minoxidil]

The mechanism by which minoxidil promotes hair growth is not fully understood. Minoxidil contains the nitric oxide chemical moiety and may act as a nitric oxide agonist. Similarly, minoxidil is a potassium channel opener, causing hyperpolarization of cell membranes. Minoxidil is less effective when there is a large area of hair loss. In addition, its effectiveness has largely been demonstrated in younger men who have experienced hair loss for less than 5 years. Minoxidil use is indicated for central (vertex) hair loss only.[4] Minoxidil is also a vasodilator.[5] Hypothetically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the follicle. This may cause follicles in the telogen phase to shed, which are then replaced by thicker hairs in a new anagen phase.

Rifampin: mechanisms of action

Rifampin specifically inhibits bacterial RNA polymerase, the enzyme responsible for DNA transcription, by forming a stable drug-enzyme complex with a binding constant of 10(-9) M at 37 C. The corresponding mammalian enzymes are not affected by rifampin. Bacterial resistance to rifampin is caused by mutations leading to a change in the structure of the beta subunit of RNA polymerase. Such resistance is not an all-or-nothing phenomenon; rather, a large number of RNA polymerases with various degrees of sensitivity to rifampin have been found. No strict correlation exists between enzyme sensitivity and MIC values, since inhibition of RNA synthesis does not always show up to the same extent in the two different test systems used for the determination of these values.

Mechanism griseofulvan
The drug binds to tubulin, interfering with microtubule function, thus inhibiting mitosis. It binds to keratin in keratin precursor cells and makes them resistant to fungal infections. It is only when hair or skin is replaced by the keratin-griseofulvin complex that the drug reaches its site of action. Griseofulvin will then enter the dermatophyte through energy dependent transport processes and bind to fungal microtubules. This alters the processing for mitosis and also underlying information for deposition of fungal cell walls.

Mechanism of action imipramine

Imipramine, tertiary amine, affects numerous neurotransmitter systems known to be involved in the etiology of depression, anxiety, ADHD, enuresis and numerous other mental and physical conditions. Imipramine is similar in structure to some muscle relaxants, and has a significant analgesic effect and, thus, is very useful in some pain conditions.

Mechanism of action of isosorbide dinitrate Similar to other nitrites and organic nitrates, isosorbide dinitrate is converted to nitric oxide (NO), an active intermediate compound which activates the enzyme guanylate cyclase (atrial natriuretic peptide receptor A). This stimulates the synthesis of cyclic guanosine 3',5'monophosphate (cGMP) which then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation Mechanism of action of tolbutamide Sulfonylureas lower blood glucose in patients with NIDDM by directly stimulating the acute release of insulin from functioning beta cells of pancreatic islet tissue by an unknown process that involves a sulfonylurea receptor (receptor 1) on the beta cell. Sulfonylureas inhibit the ATP-potassium channels on the beta cell membrane and potassium efflux, which results in depolarization and calcium influx, calcium-calmodulin binding, kinase activation, and release of insulin-containing granules by exocytosis, an effect similar to that of glucose
Mechanism of action of ranitidine

The H2 antagonists are competitive inhibitors of histamine at the parietal cell H2 receptor. They suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid. They accomplish this by two mechanisms: histamine released by ECL cells in the stomach is blocked from binding on parietal cell H2 receptors which stimulate acid secretion, and other substances that promote acid secretion (such as gastrin and acetylcholine) have a reduced effect on parietal cells when the H2 receptors are blocked.

Definitions: Optical Isomers

Optical isomers are molecules that differ three-dimensionally by the placement of substituents around one or more atoms in a molecule. Optical isomers were given their name because they were first able to be distinguished by how they rotated plane-polarized light. These molecules are not necessarily locked into their positions, but cannot be converted into one another, even by a rotation around a single bond. For example, consider the following two molecules.

In the molecule on the left, the chlorine is oriented upward, and in the molecule on the right, the chlorine is oriented downward. (These molecules are presented in Wedge-Dash Notation, which will be covered in more detail in a later section in the tutorial. To learn about this notation now, click here. To navigate back

to this page from the Wedge-Dash information page, use the Back button in the browser, not within the tutorial.) These structures can be viewed from a different angle, using Newman Projections, as shown below. (Converting between two different types of structural representations is complicated and will be covered in detail in a later section. For now, simply note that in the above structures, the chlorines were opposites in the sense of being "up" and "down," and now they are opposites in the sense of being "left" and "right.")

Geometric Isomerism

Geometric Isomerism results most commonly from Carbon-Carbon double bonds.

The important property which introduces the feature is the inability of the Carbon atoms to rotate relative to one another about the double bond. This is due specifically to the Pi bond but I won't discuss this part of the subject further on this site. The lack of rotation means the same groups can be attached in different ways to achieve diastereomers. The molecules have identical connectivity so can't be described as structural isomers.

Conformational isomerism
In chemistry, conformational isomerism is a form of stereoisomerism in which the isomers can be interconverted exclusively by rotations about formally single bonds (refer to figure on single bond rotation).[1] Such isomers are generally referred to as conformational isomers or conformers and, specifically, as rotamers.[2] Rotations about single bonds are restricted by a rotational energy barrier which must be overcome to interconvert one conformer to another. Conformational isomerism arises when the rotation about a single bond is relatively unhindered. That is, the energy barrier must be small enough for the interconversion to occur. Conformational isomers are thus distinct from the other classes of stereoisomers (i. e. configurational isomers) where interconversion necessarily involves breaking and reforming of chemical bonds.[3] For example, L- & D and R- & S- configurations of organic molecules have different handedness and optical activities, and can only be interconverted by breaking one or more bonds connected to the chiralatom and reforming a similar bond in a different direction or spatial orientation.

The study of the energetics between different rotamers is referred to as conformational analysis.[4] It is useful for understanding the stability of different isomers, for example, by taking into account the spatial orientation and through-space interactions of substituents. In addition, conformational analysis can be used to predict and explain product(s) selectivity, mechanisms, and rates of reactions