However, multiple factors can influence metabolism. Half-life is reduced by up to 50% in smokers compared to nonsmokers. The half-life of caffeine is approximately 5 hours in the average adult. These metabolites are then further metabolized and excreted in the urine. Metabolism results in 1 of 3 dimethylxanthine, including paraxanthine, theobromine, and theophylline, each with unique effects on the body. Metabolism of caffeine primarily occurs in the liver via the cytochrome P450 oxidase system, specifically enzyme CYP1A2. It is also a potent stimulator of gastric acid secretion and gastrointestinal (GI) motility. Caffeine increases renal blood flow, glomerular filtration, and sodium excretion resulting in diuresis. įurthermore, adenosine receptor blockage stimulates respiratory drive by increasing medullary ventilator response to carbon dioxide, stimulating central respiratory drive, and improving diaphragm contractility. However, there is little to no acute effect on habitual consumers. Overall, caffeine seems to increase systolic blood pressure by approximately 5 to 10 mmHg in individuals with infrequent use.
As there are multiple constriction and dilatation mechanisms at work, the overall result is individualized and dependent upon caffeine dose, the frequency of use, and comorbidities such as diabetes or hypertension. This vasodilation becomes counteracted by increased sympathetic tone via catecholamine release and positive cardiac inotropic and chronotropic effects, promoting vasoconstriction. This action promotes further relaxation of vascular smooth muscle cells.
At the vascular level, caffeine undergoes a complex interaction to control vascular tone, which includes direct antagonism of vascular adenosine receptors to promote vasodilation, as well as stimulation of endothelial cells to release nitric oxide. Likewise, adenosine receptor antagonism stimulates the release of catecholamines, contributing to the systemic stimulatory effects of caffeine and further stimulating cardiac inotropy and chronotropy. In cardiac muscle, direct antagonism of receptor A1 results in positive inotropic effects. Īdenosine receptors are not limited to the CNS but are present throughout the body. Specifically, the antagonism of the A2a receptor is responsible for the wakefulness effects of caffeine.
As it is both fat and water-soluble, it readily crosses the blood-brain barrier, resulting in antagonism to all four adenosine receptor subtypes (A1, A2a, A2b, A3). Ĭaffeine’s primary mechanism of action is on the adenosine receptors in the brain. It is also under investigation for its efficacy in treating depression and neurocognitive declines, such as those seen in Alzheimer and Parkinson disease. Caffeine has links with decreased all-cause mortality. Non-FDA-approved uses of caffeine include treating migraine headaches and post-dural puncture headaches and enhancing athletic performance, especially in endurance sports. The FDA has approved caffeine for use in the treatment of apnea of prematurity and prevention and treatment of bronchopulmonary dysplasia of premature infants. The primary goal of caffeine consumption is to combat fatigue and drowsiness, but there are many additional uses. It is also an additive to soda and energy drinks. This drug is most commonly sourced from the coffee bean but can also be found naturally occurring in certain types of tea and cacao beans. Caffeine is a naturally occurring central nervous system (CNS) stimulant of the methylxanthine class and is the most widely taken psychoactive stimulant globally.
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