Adenosine is an endogenous, essential for energy metabolism nucleoside, which is composed of the purine base adenine and β-D-ribose. It is the basic building block of adenosine triphosphate (ATP), a major source of energy for all tissue cells of the human organism.
In all energy-consuming cell processes ATP is reduced to ensure energy demand and released its building block adenosine. The Adensosinkonzentration in the blood increases accordingly under physical stress strongly.
In addition, adenosine is a component of ribonucleic acids (DNA building blocks), coenzymes and nucleoside antibiotics. Adenosine has a similar molecular structure to caffeine and occupies the same receptors but does not stimulate them. The physiological half-life is extremely short with just a few seconds.
Adenosine performs important functions in the human organism. Thus, it serves as an important component of ATP for the regeneration of the main energy store involved in all cellular processes. Adenosine is released from the nerve cells whenever the energy supply to the neurons is no longer sufficiently ensured.
This is the case, inter alia, in an ischemia (reduced blood flow). In contrast to neurotransmitters (biochemical messengers), the release is not mediated by the exocytosis of storage vesicles but by transport proteins. The transport proteins then also remove the liberated adenosine from the extracellular space. In ischemia there is an increased adenosine concentration in the intracellular space, which causes a transport reversal. When released ATP is degraded by ectoenzymes (enzymes outside the cell), the extracellular adenosine concentration also increases.
In the nervous system, adenosine occupies the receptors provided for caffeine and the neurotransmitters dopamine, norepinephrine and acetylcholine, thereby blocking their action. The more active the nerve cells are, the higher the ATP and thus adenosine concentration. By occupying the receptors, the function of the nerve cells is slowed down and the nervous system is protected from overexertion. As a result of this neurotransmitter blockade, the blood vessels are dilated (dilatation). There is a consecutive drop in blood pressure (lowering blood pressure) and a slowing of the heart rate.
Activation of the G protein-modulated potassium channels (via A1 adenosine receptors) also prolongs the conduction time in the AV node (atrioventricular node). As the secondary pacemaker of the heart, the AV node is the only connection between the atrium and ventricle (ventricle) and regulates the excitation conduction into the ventricles.
The delayed transmission of the stimulus ensures a coordinated contraction of the ventricle and the atrium. As the adenosine concentration increases with exercise and oxygen deficiency, it is believed that the increased release prevents inefficient tachycardia and cardiac arrhythmias under stress.
Adenosine is primarily used as an antiarrhythmic drug for the treatment of cardiac arrhythmias. Due to the very short half-life in the blood, adenosine can be administered as a short infusion intravenously to control the blood pressure (blood pressure reduction) and the heart rhythm (3, 6 or 12 mg).
In addition to the dilation of the peripheral vessels, adenosine additionally dilates the coronary arteries. Adenosine can terminate AV node-dependent tachycardia by blocking AV conduction, making it the drug of first choice, especially in supraventricular tachycardias such as AV nodal reentrytachycardia.
In addition, atrial tachycardias such as paroxysmal tachycardia (sudden onset of heart rate acceleration) can be treated with adenosine. Similarly, adenosine is used in diagnostics in stress studies for dilatation of the cardiac vessels (imaging of the heart).
Heart adenosine increased locally by ischemia may cause bradycardia (bradycardia). Theophylline as an antidote inhibits adenosine activity at the corresponding receptor of the heart.
In addition, therapeutically applied adenosine due to its negative dromotropic effect (slowing down the transmission of excitation) cause a short-term asystole (missing myocardial contraction). In these cases, adenosine intakes should be discontinued immediately. Due to the short half-life, the pharmacological effect sounds very fast.
As a result of the vasodilator effect, flushing symptoms characterized by brief erythema may occur. In addition, difficulty breathing, chest pressure, headache, dizziness, nausea and tingling sensation may occur in the short term if adenosine is injected. The use of adenosine is contraindicated in bronchospasm, COPD and bronchial asthma. Tags: