Biochemically, prostaglandins belong to the eicosanoids. They are a kind of precursor of arachidonic acid consisting of quadruple unsaturated fatty acids with 20 carbon atoms. Their special feature lies in the mediation of pain, in the processes of inflammatory reactions and the development of fever.
Prostaglandins consist of several subgroups. The prostaglandin E2 (PGE 2) should be emphasized here, since it has an important physiological significance as a local hormone, i.e. as a tissue hormone. The production site or biosynthesis of eicosanoids, i.e. also of prostaglandins, takes place in the endoplasmic reticulum (ER) of a cell.
Prostaglandin E2 is produced in particular during stimulation by inflammatory reactions by cells of the immune system, such as macrophages or monocytes. Immature blood platelets (thrombocytes) are also stimulated by prostaglanidin E2 to differentiate and mature. In prostaglandins, signal transduction occurs via special membrane receptors (so-called G-protein coupled receptors). Prostaglandins are found in the entire organism. A particularly high number is found in sperm, i.e. in the secretion of the prostate, which led to the naming of the hormone.
Effect of prostaglandins
Prostaglandins primarily influence the so-called second messenger system, a molecular message exchange between cells. Therefore their effect in the organism is manifold. The different subgroups of prostaglandins have different effects.
In the nervous system, for example, prostaglandins are both inhibiting and promoting the transmission of excitation to sympathetic nerve endings (part of the autonomic nervous system, see: sympathetic nervous system). Due to their chemical structure, prostaglandins are relatively unstable, which is important for their temporary effect. On the one hand, prostaglandins act directly, as is the case with smooth muscle contraction, but on the other hand they fulfill their more important function indirectly as hormone or neurotransmitters.
This is also where the effects of most drugs with regard to prostaglandins start. Since prostaglandins are involved in inflammatory processes and in the development of fever and pain, attempts are made to intervene in the metabolism by means of so-called cyclooxygenase inhibitors. This leads to prostaglandin inhibition and thus to an alleviation of symptoms.
Probably the best known drug that works according to this principle is acetylsalicylic acid, known as aspirin. In the kidney, prostaglandin E2 (PGE2) is the most important prostaglandin. Although it is produced in the renal cortex, the renal medulla produces many times more PGE2.
The physiologically most important function of PGE2 in the kidney is vasodilation and an increase in blood flow. PGE2 increases the release of the hormones renin and prostacyclin in the cells of the renal corpuscles. Renin is an important component of the renin-angiotensin-aldosterone system (RAAS).
This system significantly regulates the fluid or electrolyte balance of the organism and is therefore a central unit for regulating blood pressure. However, this can also lead to diseases. In the so-called Bartter Syndrome there is an increased release of prostaglandin E2 and thus an overactivity of the RAAS described above.
Urinary excretion provides evidence of the formation of PGE2 in the kidney. It should also be noted that diseases such as heart failure or renal insufficiency severely restrict the blood supply to the kidney and thus its functional activity. Due to an inhibition of prostaglandin synthesis, when affected patients ingest, for example, acetylsalicylic acid or diclofenac (NSAID), this functional limitation can be aggravated.
The individual subgroups of prostaglandins have different functions. For example, prostaglandin E2 (PGE2) has a protective function in the stomach. The mucous membrane cells of the stomach produce prostaglandin E2.
The gastric mucus protects the stomach from gastric acid, whose production is inhibited by PGE2. This effect of PGE2 is basically based on three mechanisms: PGE2 greatly increases the blood supply to the stomach mucosa, which is necessary for optimal functioning. PGE2 reduces the secretion of gastric acid by the lining cells of the stomach wall.
Secondary cells produce mucus in the stomach. This mucus secretion is increased by PGE2. These three mechanisms explain why drugs such as acetylsalicylic acid (see: Aspirin) can lead to repeated gastric bleeding or ulcers (peptic ulcers) as a result of increased consumption.Acetylsalicylic acid is a cyclooxygenase 1 inhibitor (COX1 inhibitor), which limits or prevents the protective function of prostaglandins.
- PGE2 greatly increases the blood flow to the stomach lining, which is necessary for optimal function.
- PGE2 reduces the secretion of gastric acid by the lining cells of the stomach wall.
- Side cells produce mucus in the stomach. This mucus secretion is increased by PGE2.