Atropine Pharmacokinetics Atropine Has Many

Atropine Pharmacokinetics Atropine has many different uses for individuals, because of its great effect on the body. Although the direct effect and the length of time that it takes for atropine to function differs according to how the drug is administered, the basis is very similar. To begin, once the drug has been administered, its target is a muscarinic acetylcholine receptor. These receptors function by receiving acetylcholine in order for the parasympathetic system to function correctly.

However, once atropine is in the body, it is a competitive antagonist for these muscarinic acetylcholine receptors (Katzung, Masters, & Trevor, 2012). The antagonist is a molecule in atropine that inhibits the agonists' (in this case the agonist is acetylcholine) actions by preventing acetylcholine from binding to the active site and initiating the conformational change necessary for its targets to be initiated. After atropine binds to the receptor, it is reversibly bound, so it does not stabilize the conformational change on the receptor, so no activation actually occurs.

Because of this, the receptors are occupied, but no action is taking place because acetylcholine cannot bind and cause the targeted action. This leads to a build-up of acetylcholine in the body system (Katzung, Masters, & Trevor, 2012). After binding, atropine diffuses into the cell and eventually into the bloodstream. This most directly affects the vagus nerve which is the primary cranial nerve in charge of the parasympathetic system.

Blocking the acetylcholine from binding, which is what atropine is essentially doing, will then promote a variety of effects on an individual's body that are the complete opposite of what the vagus nerve would have initially started. Atropine will vasodilate the blood vessels, increase the electroconductivity of the AV node, and as a result, do what it is supposed to: increase heart rate in individuals.

The digestive system will also be slowed down as the main ingredient for the "rest and digest" process of the parasympathetic system will be missing (Katzung, Masters, & Trevor, 2012). Without any acetylcholine receptors available to bind acetylcholine, the effects on the body will counteract that of the parasympathetic system. After atropine has prevented acetylcholine from binding and has produced its effects on the body, it will then need to be removed from the body so as to not be constantly blocking the muscarinic receptors.

This would mean that if the atropine isn't metabolized and then excreted, a constant influx of acetylcholine would build up, causing lethal effects on the individual (Katzung, Masters, & Trevor, 2012). The body alters the drug in Phase I and Phase II through oxidation by adding a hydroxyl group to the atropine molecule in order to make it hydrophilic, allowing it to travel to the renal system for excretion for rapid and successful elimination.

While half of the atropine drug is metabolized and hydrolyzed to tropine and tropic acid, half of it is excreted unchanged through the renal and urinary system. Atropine follows the cytochrome P450 enzyme system, so in order for excretion to occur, the drug needs to go through renal glomerular filtration as the blood is being filtered, secreted into the proximal tubular where more wastes are gotten rid of, and finally reabsorbed into the tubular lumen where.