Discussion of all aspects of cellular structure, physiology and communication.
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Hi! I have a question about the effectiveness of painkillers. How does painkillers work? I believe it has something to do with the cells receptors, but I don't know what's actually happening when I consume an Aspirin, for instance. can someone please explain? What is the reason for tolerance? what cell biological functions are trigged resulting in a more or less tolerance against a painkiller drug?
I'm very grateful for any answers.
Best regards, Nelsson.
it depends on the painkiller. but here is a crash course
Pain is caused by the release in some special cases of paracrine hormones named prostaglandines. These hormones then trigger the physiological state of pain. Aspirin and ibuprofen inhibit the first enzyme in prostaglandin synthesis, named cyclooxigenase(COX) or prostaglandin H2 synthase more formally. However, you need to understand that prostaglandins do many more things than just inflict pain. For example they signal the production of stomach mucus, which is the reason large quantities of aspirin will cause stomach aches.
Tolerance to drugs appears from generally the same reason: the oxidative enzymes in the smooth endoplasmic reticulum of liver cells grow in number, and even the RE can be seen to expand under the microscope. Therefore, they are degraded much quicker.
If you have any specific questions, ask away
"As a biologist, I firmly believe that when you're dead, you're dead. Except for what you live behind in history. That's the only afterlife" - J. Craig Venter
nice. thank you very much:) I have a few more questions though. Does prostaglandin synthesis occur at one specific place in our body, and thereby aspirin inhibiting this one reaction? I mean, aspirin ease several different kinds of pain, how is this possible?
prostaglandin synthesis occurs locally, where the pain occurs. google for "paracrine hormone" to find out more. Aspirin inhibits the syntehsis everywhere cause it travels through the blood
6 posts • Page 1 of 1
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