Prostaglandins are signaling molecules your body produces on demand to regulate pain, inflammation, fever, blood clotting, stomach protection, and reproductive functions. Unlike traditional hormones that travel through the bloodstream from a specific gland, prostaglandins are made by nearly every cell in the body and act locally, with a very short half-life. This means they do their work right where they’re produced, then break down quickly.
How Your Body Makes Prostaglandins
Prostaglandins start as arachidonic acid, a fatty acid sitting in your cell membranes. When a cell is damaged, stimulated, or receives the right chemical signal, enzymes pull arachidonic acid free. From there, two key enzymes called COX-1 and COX-2 convert it into different types of prostaglandins, each with distinct roles.
COX-1 runs continuously in most tissues, producing the prostaglandins needed for everyday maintenance: protecting your stomach lining, supporting kidney function, and helping platelets in your blood work properly. COX-2, on the other hand, is mostly quiet until something goes wrong. It ramps up at sites of inflammation, injury, or infection, flooding the area with prostaglandins that trigger swelling, pain, and fever. This distinction between the two enzymes is the reason different pain medications have different side effects.
Pain and Inflammation
Prostaglandins don’t directly cause pain the way a cut or burn does. Instead, they lower the threshold at which your nerve endings fire, making them respond to stimuli that normally wouldn’t hurt. At concentrations as low as nanomolar levels, prostaglandins sensitize nerve cells both at the injury site (peripheral sensitization) and in the spinal cord (central sensitization). The result is a state where normally non-painful pressure or temperature can become genuinely painful.
They accomplish this by changing how ion channels on nerve cells behave. One well-studied effect: prostaglandin E2 shifts the activation curve of certain sodium channels on sensory neurons, making those neurons fire more easily and more often. Prostaglandins also amplify the activity of heat-sensing receptors on nerve endings, which is part of why inflamed tissue feels hot and tender to the touch. Alongside this nerve sensitization, prostaglandins widen local blood vessels and increase their permeability, producing the redness and swelling that characterize inflammation.
Fever
When your immune system detects an infection, it releases signaling molecules that trigger COX-2 activity in the brain. The prostaglandin E2 produced there binds to specific receptors in the preoptic hypothalamus, the brain region that acts as your internal thermostat. Under normal conditions, neurons in this area send constant inhibitory signals that keep your body temperature stable. When prostaglandin E2 silences those neurons, the brakes come off, and your brain activates heat-generating pathways: shivering, blood vessel constriction in the skin, and increased metabolic activity. Your temperature rises, and you have a fever.
This is why common pain relievers reduce fever. By blocking COX enzymes, they cut off prostaglandin E2 production in the brain, allowing the hypothalamus to resume its normal temperature regulation.
Blood Clotting and Vessel Tone
Two prostaglandin-related molecules play opposing roles in your blood vessels, and their balance is critical. Thromboxane A2, produced mainly by platelets, constricts blood vessels and promotes clot formation. Prostacyclin, produced by the cells lining blood vessel walls, does the opposite: it relaxes vessels and prevents platelets from clumping together.
In a healthy system, these two forces stay in equilibrium. When you cut yourself, thromboxane helps form a clot to stop bleeding. Prostacyclin prevents that clotting process from spreading beyond where it’s needed. When this balance is disrupted, problems follow. An excess of thromboxane relative to prostacyclin increases the risk of dangerous clots, which is one reason low-dose aspirin (which preferentially reduces thromboxane production in platelets) is sometimes used to lower cardiovascular risk.
Stomach and Kidney Protection
Prostaglandins play a surprisingly important housekeeping role in the stomach. They suppress acid secretion, dilate blood vessels in the stomach wall to maintain blood flow, and stimulate the production of the thick mucus layer that keeps stomach acid from digesting the stomach itself. In animal studies, even tiny doses of prostaglandins administered before exposure to damaging substances provided striking protection against stomach injury.
This protective role explains one of the most common side effects of anti-inflammatory drugs. Because these medications block COX enzymes throughout the body, they reduce prostaglandin production in the stomach along with the prostaglandins causing pain. The result is less mucus, less blood flow to the stomach lining, and a higher risk of ulcers and gastrointestinal bleeding, especially with long-term use.
In the kidneys, prostaglandins help regulate blood flow to the filtering units and control how much sodium and water your body retains. Prostaglandin E2 specifically influences salt transport in a key part of the kidney. When anti-inflammatory drugs suppress this function, sodium reabsorption increases, which can cause fluid retention, swelling in the ankles, and worsened blood pressure.
Reproduction and Labor
Prostaglandins are central to reproductive function in both men and women. During menstruation, prostaglandin levels in the uterine lining rise sharply, triggering the contractions that shed the lining. Women who produce higher levels of prostaglandins tend to experience more intense menstrual cramps, which is why anti-inflammatory medications are effective for period pain.
In pregnancy, prostaglandins help initiate labor by softening and stretching the cervix through their effect on cervical collagen, and by stimulating uterine contractions. This role is so well established that synthetic prostaglandin preparations are routinely used in hospitals to ripen the cervix and induce labor when medically necessary. Even semen contains prostaglandins, which is the basis for the common suggestion that sexual intercourse near a due date could help trigger labor onset.
How Anti-Inflammatory Drugs Work Against Them
Non-steroidal anti-inflammatory drugs, or NSAIDs, work by blocking COX enzymes, cutting off prostaglandin production at the source. This reduces pain, fever, and inflammation, but because prostaglandins do so many things, the effects ripple across multiple organ systems.
Blocking COX-1, the “housekeeping” enzyme, is what causes stomach irritation, reduced kidney blood flow, and changes in platelet function. Medications designed to selectively block only COX-2 were developed to spare the stomach, but they introduced a different problem: by reducing prostacyclin without equally reducing thromboxane, they shifted the clotting balance and increased cardiovascular risk. Prostaglandin inhibition can also affect bone metabolism, since prostaglandins help regulate the cells that build and break down bone. In the lungs, reduced prostaglandin production can trigger airway narrowing in susceptible people, which is why some individuals with asthma are sensitive to aspirin.
Medical Uses of Synthetic Prostaglandins
Because prostaglandins have so many specific functions, synthetic versions have been developed to target individual conditions. Prostaglandin-based eye drops are a first-line treatment for glaucoma, lowering pressure inside the eye. One of these compounds also has an FDA approval for growing longer, thicker eyelashes, a cosmetic effect discovered as a side effect during glaucoma treatment.
A synthetic prostaglandin E1 is approved for preventing stomach ulcers in people who need to take anti-inflammatory drugs long-term, essentially replacing the stomach protection those drugs eliminate. The same compound is widely used off-label in obstetrics for cervical ripening and labor induction. Other prostaglandin-based medications treat pulmonary arterial hypertension by relaxing blood vessels in the lungs, manage severe postpartum bleeding by promoting uterine contraction, treat erectile dysfunction by dilating blood vessels, and in one case, reduce the risk of digit amputation from severe frostbite by restoring blood flow.
Prostaglandins are also used in newborns with certain congenital heart defects. Some of these infants depend on a small blood vessel called the ductus arteriosus remaining open until surgery can be performed. A synthetic prostaglandin keeps this vessel from closing, buying critical time.