Caffeine is though to produce a pharmacological action by antagonising adenosine receptors. In addition, caffeine can inhibit phosphodiesterase, which increases cellular cyclic AMP and causes a subsequent stimulation of the catecholamine hormonal system. The result of these interactions is a complex cardiovascular response that can increase blood pressure in some individuals. The effects of caffeine on blood pressure has been extensively researched but the results of studies have generally been inconsistent. A large biochemical variability between subjects has been reported as the likely cause. Just as with sodium, it appears that a number of individuals respond to caffeine ingestion with increased blood pressure. These individuals may bias study results to show a positive association between caffeine intakes and blood pressure, depending on the sample size and the number of responders included. The large between subject variability of caffeine metabolism suggests a genetic component.
Research has shown that there exists a large variability in the cytochrome P450 1A2 (CYP1A2) metabolism of caffeine, that accounts for around 95% of caffeine metabolism. However, less is known about how gene variants for the adenosine or catecholamine receptors alter caffeine metabolism. Recent research suggests that polymorphism in these genes may be a contributory cause of the between subject variability in blood pressure seen following caffeine intake. Researchers1 investigated acute (<2 hour) blood pressure responses to caffeine in relation to variation in adenosine and adrenaline receptor genes in 110 healthy males coffee drinkers. Subjects consuming normal coffee responded with an increase in mean systolic blood pressure (4 mm Hg), diastolic blood pressure (3 mm Hg) and plasma adrenaline, when compared to decaffeinated coffee. Associations were observed for polymorphisms between both ADORA2A TT and ADRA2B I, and systolic blood pressure, in response to caffeine.
The ADORA2A TT and ADRA2B I genes code for the adenosine A2A receptor and the α2B-adrenergic receptor, respectively. These results therefore suggest that polymorphisms in the A2A adenosine receptor and α2-adrenergic receptors may explain the between subject variability in blood pressure seen with caffeine consumption. Therefore caffeine drinking may affect the cardiovascular system in individuals who show these polymorphisms, through small elevations in blood pressure. The fact that this study used habitual coffee drinkers shows that blood pressure elevation is not limited to those who are sensitive to the effects of caffeine, but occur in those who are desensitised through regular consumption. Interestingly, there was no association between blood pressure changes and the CYP1A2 gene. However, the 2 hour time frame of this study may have been too short to evaluate caffeine metabolism, as responses from slow and fast metabolisers could manifest after the 2 hour period.
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