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PubMed1985

Effects of maternal caffeine intake on the growth of rat tooth germs in protein-energy malnourished neonates.

Fourteen rat dams with 8 pups each were fed either a 6, 12 or 20 per cent protein diet upon birth. Another group of 12 dams with the same number of pups was pair-fed either a 6, 12 or 20 per cent protein diet supplemented with caffeine (2 mg/100 g body weight). At day 15, randomly-selected pups were injected with [14C]-proline to determine collagen synthesis of the incisor and molar tooth germs. Another group of pups was used to determine calcium content of these tooth germs. Body weight, incisor weight and total calcium contents of tooth germs of pups from dams fed with 6 per cent protein diet were greater in the caffeine-supplemented group, whereas in the 20 per cent protein diet with caffeine group, these parameters were lower. The molar weights of the 12 per cent protein diet with caffeine animals were greater than the 12 per cent group without caffeine. The total hydroxyproline content of the incisor tooth germs from animals in the 12 per cent protein diet with caffeine was greater than is the non-caffeine group. However, total hydroxyproline of the molar tooth germs in the 20 per cent protein groups with caffeine was less than in the non-caffeine group. The rate of collagen synthesis of the incisor and molar tooth germs showed no difference in the presence or absence of caffeine in the 6, 12 and 20 per cent protein groups. Incisor and molar tooth germs are thus affected differently by the interaction of protein and caffeine, possibly due to differences in the pattern of tooth development.

Animals↗
PubMed1986

The mechanism of caffeine-enhanced glucose stimulation of liver glycogen synthase phosphatase activity.

Our report that glucose within its physiological range stimulates glycogen synthase phosphatase activity, provided an appropriate second effector is present, has been expanded. The nature of the stimulatory process, particularly the roles of glucose, and of caffeine which represents the potential second effectors, has been studied. Glucose and caffeine stimulated synthase phosphatase activity in a synergistic manner. With 0.5 mM caffeine the A0.5 for glucose was 11 mM (from 27 mM), whereas in the presence of 30 mM glucose the A0.5 for caffeine was 0.06 mM (from 0.7 mM). At 10 mM glucose the A0.5 for caffeine was 0.1 mM. Glucose stimulation remained non-cooperative, unaffected by the presence of caffeine, whereas the cooperative stimulation of caffeine was unaffected by glucose. Some slight stimulation of synthase activity was observed with caffeine and with glucose over a wide concentration range. However, they did not act synergistically to influence the measurement of synthase activity. Glucose-6-phosphate, which also stimulates synthase phosphatase activity, acted independently, not synergistically with caffeine. All the methylxanthines were tested as potential second effectors in an effort to discover the essential structural elements of the agent. All dimethylxanthines, 3- and 7-methylxanthine and 1-methyl-3-isobutylxanthine enhanced glucose stimulation but none of them alone was stimulatory. Judged from the half-maximal concentrations, in the presence of 10 mM glucose, caffeine was the most potent second effector by a significant margin. The maximum velocity was also greatest with caffeine, whereas that with other methylxanthines was generally lower, and varied. 1-Methylxanthine with increased concentration was slightly inhibitory even in the presence of 10 mM glucose. Xanthine (0.5 mM), itself, strongly inhibited synthase phosphatase activity, an effect not influenced by glucose. Xanthine did not influence the measurement of synthase or phosphorylase phosphatase activity with or without glucose. In general, conditions of methylxanthine-enhanced, glucose stimulation of synthase phosphatase and phosphorylase phosphatase activities differed markedly, confirming that separate, distinct mechanisms are involved.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Synergistic release of calcium in sea urchin eggs by caffeine and ryanodine.

A transient rise in intracellular Ca2+ during fertilization is necessary for activation of the quiescent sea urchin egg. Several mechanisms contribute to the rise in Ca2+ including influx across the egg plasma membrane and release from intracellular stores. The egg contains both IP3-sensitive and -insensitive Ca2+ release mechanisms and in this study we have used single-cell spectrofluorimetry to examine the effects of caffeine and ryanodine on Ca2+ release in eggs preloaded with fura 2. Caffeine induced a small Ca2+ release that was insensitive to heparin or ruthenium red. Ca2+ liberation by caffeine could be augmented by prior treatment with thapsigargin, an inhibitor of endoplasmic reticulum Ca2+ ATPase. Variable Ca2+ releases were observed in response to microinjection of ryanodine. The action of ryanodine appeared to be enhanced by prior injection of heparin and partially inhibited by ruthenium red. The release of Ca2+ by caffeine or ryanodine was generally insufficient to trigger cortical granule exocytosis, thus these eggs could be fertilized and a second Ca2+ release during fertilization was measured. Unlike the caffeine- and ryanodine-sensitive Ca(2+)-induced Ca2+ release mechanism in somatic cells, the graded responses in eggs suggested this caffeine- and ryanodine-sensitive release mechanism is not sensitive to sudden changes in Ca2+. Thus we could examine the combined actions of caffeine and ryanodine on Ca2+ release, which were synergistic. Caffeine treatment of ryanodine-injected eggs or ryanodine injection of caffeine-treated eggs stimulated a Ca2+ release significantly larger than the release by either drug independently. The experiments presented here suggest that sea urchin eggs liberate Ca2+ in response to caffeine and ryanodine; however, the regulation of this release differs from that described for caffeine- and ryanodine-sensitive Ca(2+)-induced Ca2+ release of somatic cells.

Animals↗
PubMed1984

Protein-energy malnutrition during pregnancy alters caffeine's effect on brain tissue of neonate rats.

We studied whether protein-energy malnutrition changed brain susceptibility to a small dose of caffeine in newborn rats. Since we had demonstrated previously that caffeine intake during lactation increased the brain neuropeptide on newborns, we investigated further the effects of the prenatal administration of caffeine on TRH and cyclo (His-Pro). From day 13 of gestation to delivery day, pregnant rats in one group were fed either a 20% or a 6% protein diet ad libitum, and those in the other group were pair-fed with each protein diet supplemented with caffeine at an effective dose of 2 mg/100 g body weight. Upon delivery, brain weight, brain protein, RNA, DNA and the neuropeptides thyrotropin-releasing hormone (TRH) and cyclo (His-Pro) were measured in the newborn rats. A 6% protein without caffeine diet caused reductions in brain weights and brain protein, RNA and DNA contents, but did not alter brain TRH and cyclo (His-Pro) concentrations in the newborn animals. In the offspring from dams fed a 6% protein diet, caffeine administration significantly elevated brain weights and brain contents of protein, RNA and DNA. In contrast, these values were similar between noncaffeine and caffeine-supplemented animals in a 20% protein diet group. Brain TRH and cyclo (His-Pro) concentrations were not changed by caffeine administration. These data suggest that caffeine augments protein synthesis in the newborn rat brain when malnourished, but that the same dose of caffeine did not affect protein synthesis in brains of newborn rats from normally nourished dams. Therefore, the present findings indicate that the nutritional status of mothers during pregnancy has important implication in the impact of caffeine on their offspring's brains.

Adult↗
PubMed1985

Caffeine tolerance: behavioral, electrophysiological and neurochemical evidence.

The development of tolerance to the stimulatory action of caffeine upon mesencephalic reticular neurons and upon spontaneous locomotor activity was evaluated in rats after two weeks of chronic exposure to low doses of caffeine (5-10 mg/kg/day via their drinking water). These doses are achievable through dietary intake of caffeine-containing beverages in man. Concomitant measurement of [3H]-CHA binding in the mesencephalic reticular formation was also carried out in order to explore the neurochemical basis of the development of tolerance. Caffeine, 2.5 mg/kg i.v., markedly increased the firing rate of reticular neurons in caffeine naive rats but failed to modify the neuronal activity in a group exposed chronically to low doses of caffeine. In addition, in spontaneous locomotor activity studies, our data show a distinct shift to the right of the caffeine dose-response curve in caffeine pretreated rats. These results clearly indicate that tolerance develops to the stimulatory action of caffeine upon the reticular formation at the single neuronal activity level as well as upon spontaneous locomotor activity. Furthermore, in chronically caffeine exposed rats, an increase in the number of binding sites for [3H]-CHA was observed in reticular formation membranes without any change in receptor affinity. We propose, therefore, that up-regulation of adenosine receptors may underlie the development of tolerance to the CNS effects of caffeine.

Action Potentials↗
PubMed1994

Enhancement of hepatic tryptophan pyrrolase activity and decreases of open field locomotion following single and repeated administration of high doses of caffeine in rats.

In view of a possible role of kynurenine in caffeine-induced anxiety syndrome, the effects of single and repeated administration of caffeine on hepatic tryptophan (T)-pyrrolase activity are investigated. Single administration of caffeine at doses of 80 mg/kg decreased open field locomotion and increased hepatic T-pyrrolase activity. Locomotor stimulating effects of 80 mg/kg caffeine, monitored in the home cages of rats, were attenuated following daily administration of caffeine for 5 days. Open field locomotor activity of rats and its caffeine-induced decrement were also attenuated following 5 daily administrations of caffeine on the 6th day. Basal levels of hepatic T-pyrrolase activity increased after 5 daily administrations of caffeine on the 6th day. Acute administration of caffeine did not further elevate hepatic T-pyrrolase activity in 5 day caffeine injected rats. Drug adjuvants decreasing hepatic T-pyrrolase activity may prove valuable for extending the clinical utility of caffeine.

Animals↗
PubMed1995

Effects of acute caffeine ingestion and menopause on sulfate homeostasis in women.

Inorganic sulfate is a physiological anion which is utilized in the metabolism of both endogenous compounds and xenobiotics. Its homeostasis is maintained predominantly by facilitated reabsorptive processes in the kidneys. The objectives of the present investigation were to evaluate the effects of menopausal status and caffeine ingestion on the serum concentrations and clearance of inorganic sulfate. Thirty-nine women who were classified as premenopausal, postmenopausal with or without estrogen treatment, and postmenopausal with osteoporosis participated in the study. The women were studied on two separate occasions following the ingestion of a decaffeinated beverage to which 6 mg caffeine/kg lean body mass or no caffeine was added. All women were habitual caffeine users (mean ingestion of 588 mg caffeine per day) but abstained from all caffeine sources for 2 weeks prior to the control study day. Postmenopausal women with estrogen supplementation exhibited significantly lower sulfate serum concentrations (0.24 +/- 0.02 mM vs. 0.32 +/- 0.04 mM in premenopausal women, mean +/- SD, p < 0.05) and a decreased renal reabsorption of sulfate for the control (no caffeine) period. There was no difference in serum sulfate or sulfate reabsorption in estrogen supplemented postmenopausal women, compared with women not taking estrogen. Postmenopausal women with osteoporosis had significantly lower creatinine and sulfate clearances than postmenopausal women with estrogen supplementation which may be related to their older age, or factors related to the disease process. The 6 mg/kg dose of caffeine caused a diuresis, but no change in GFR, as indicated by urine volume and creatinine clearance values, respectively. Caffeine administration resulted in an increase in the sulfate excretion rate; there was no change in sulfate serum concentrations. The results of this investigation indicate that menopause results in decreased sulfate serum concentrations that may be the consequence of a decreased renal reabsorption of sulfate. Secondly, this investigation demonstrated that caffeine ingestion increases the urinary excretion of sulfate, an effect that may be related to the diuretic effect of caffeine or due to a caffeine-induced alteration in the renal reabsorption of sulfate.

Adult↗
PubMed1980

The effect of caffeine on cell growth and metabolism of thymidine in Escherichia coli.

(1) The influence of caffeine on growth and on the metabolism of thymidine was investigated in various E. coli strains. Caffeine caused filamentous growth in all strains investigated. The caffeine effect was reversible. (2) The incorporation of thymidine into DNA was inhibited by caffeine, and the inhibition was most pronounced with bacterial cultures grown overnight in the presence of caffeine before the addition of thymidine. For cells not pretreated with caffeine the inhibitory effect of caffeine decreased with increasing concentrations of thymidine up to about 1 microM whereafter it remained constant. The effect of thymidine concentration on the inhibition was less for bacteria that had grown overnight in the presence of caffeine than for bacteria not pretreated with caffeine. (3) Caffeine inhibited thymidine kinase, but it had no effect on thymidine phosphorylase or thymidine nucleotide kinases. (4) It is suggested that caffeine interferes with uptake of thymidine, conversion of thymidine to dTTP and the DNA synthesis process itself. Filamentous growth could be the result of the inhibition of DNA synthesis.

Biological Transport, Active↗
PubMed1982

Caffeine-metabolizing capability of primary rat hepatocytes, Chinese hamster V79 cells and normal human fibroblasts in culture.

Caffeine is metabolized by primary rat hepatocytes in culture to metabolites similar to those found in rats in vivo, including 6-amino-5-[N-formylmethylamino]-1,3-dimethyluracil, one of the major caffeine metabolites produced in the rat. At a substrate-limiting level of caffeine, the rat hepatocytes metabolized 25-30% of the total added caffeine in 24 h. About 99% of the metabolites was found in the extracellular medium and rinse fractions, suggesting that on a volume basis, caffeine metabolites are in equilibrium inside and outside the cells. No detectable caffeine metabolites were produced in preparations of either Chinese hamster V79 cells, or normal human fibroblasts at caffeine concentrations from 5 microM to 5 mM. These results suggest that the varied biological effects induced by caffeine in Chinese hamster cells cannot be attributed to caffeine metabolites and further that the differential responses of Chinese hamster cells and normal human fibroblasts to caffeine are not due to qualitative or quantitative differences in caffeine metabolism in the two cell lines.

Animals↗
PubMed1988

Behavioral dependence on caffeine and phencyclidine in rhesus monkeys: interactive effects.

Five rhesus monkeys were trained to self-administer orally-delivered phencyclidine (PCP) and water under concurrent fixed-ratio (FR) 8 schedules. Liquid deliveries were contingent upon lip-contact responses on solenoid-operated drinking spouts, and food pellet delivery was contingent upon responses on a centrally-located lever. Food was available during three 1-hr periods each day under an FR 64 or FR 80 schedule. The liquids were available during three 6.5-hr periods after each food component. In the first experiment caffeine (4 or 8 mg) was added to each 6-g food pellet, and after responding stabilized, noncaffeinated pellets were substituted for the caffeinated pellets for eight days. There were no differences in food-, water- or PCP-maintained behavior due to caffeine concentration (4 vs. 8 mg/pellet) although the monkeys consumed twice as much caffeine at the higher concentration. Food-maintained responding was reliably reduced by 25-50 percent the first day of caffeine removal, and there was a recovery of responding characterized by intermittent cycles of low response rates over the next 7 days. Water and PCP intake were not systematically disrupted when caffeine access was terminated. In the second experiment the monkeys were tested with caffeinated (6 mg/pellet) and noncaffeinated pellets under conditions of PCP removal (water substitution) and reinstatement. Under both food conditions, when PCP access was terminated, pellet deliveries decreased by about 50 percent and gradually recovered over the 8-day water substitution phase. However, behavioral disruptions were more severe under conditions in which monkeys received caffeinated pellets, suggesting an interactive effect due to termination of PCP access and decreased caffeine intake. These results indicate that disruptions in operant baselines are sensitive indicators of the effects of discontinuing caffeine access; however, the severity and time course of behavioral disruptions due to caffeine removal are considerably less than after termination of PCP access.

Animals↗
PubMed1986

Relationship of chromosomal damage induced by caffeine to growth temperature and ATP level in proliferating cells.

Caffeine is known to induce chromosomal aberrations in proliferating cells when they are incubated during G2 and mitotic prophase. In the present paper, this caffeine effect has been analyzed in Allium cepa root meristems growing at different culture temperatures under steady-state kinetics. Caffeine (1-10 mM) induces chromosomal aberrations in a dose-dependent manner, and the treatment efficiency correlates linearly with the square of caffeine concentration. The efficiency of caffeine incubations, within the range 5-25 degrees C during equivalent cycle time periods has also been studied. It has been found that the lower the culture temperature, the higher the level of chromosomal aberrations. Moreover, at different temperatures, the level of chromosomal aberrations is a simple function of caffeine concentration and the ATP level. Therefore, the efficiency of caffeine treatment appears to be determined by some interaction between caffeine concentration and cellular ATP level. Our present results demonstrate that the influence of growth temperature on the chromosome-breaking effect of caffeine can be, at least partially, explained by the ATP levels during the incubation periods. In short, under different kinetics of plant cell proliferation, the ATP level, and/or something correlating with it, could explain the efficiency of caffeine in inducing chromosomal aberrations: the lower the ATP level, the higher the caffeine efficiency.

Adenosine Triphosphate↗
PubMed1995

Caffeine antinociception in the rat hot-plate and formalin tests and locomotor stimulation: involvement of noradrenergic mechanisms.

The present study examined antinociception produced by systemic administration of caffeine in the rat hot-plate (HP) and formalin tests and addressed several aspects of the mechanism of action of caffeine. Locomotor activity was monitored throughout. Caffeine produced a dose-related antinociception the HP (50-100 mg/kg) and formalin tests (12.5-75 mg/kg). When observed during the formalin test, caffeine stimulated locomotor activity between 12.5 and 50 mg/kg; this was followed by a depression in activity at 75 mg/kg. Caffeine did not produce an anti-inflammatory effect as determined by hindpaw plethysmometry, suggesting that antinociception was not secondary to an anti-inflammatory action. Peripheral co-administration of caffeine with the formalin did not produce antinociception, suggesting a predominant central rather than peripheral site of action for caffeine. Naloxone (10 mg/kg) did not reduce the antinociceptive or locomotor stimulant effects of caffeine, suggesting a lack of involvement of endogenous opioids in these actions. Phentolamine (5 mg/kg) enhanced antinociception by caffeine in both the HP and formalin tests, but inhibited locomotor stimulation. Prazosin (0.15 mg/kg) mimicked the action of phentolamine on locomotor stimulation, but idazoxan (0.5 mg/kg) mimicked the action of phentolamine on antinociception in the formalin test. These observations suggest an involvement of different alpha-adrenergic receptors in the two actions of phentolamine. Microinjection of 6-hydroxydopamine (6-OHDA) into the locus coeruleus, which depleted noradrenaline (NA) in the spinal cord and forebrain, inhibited the action of caffeine in the HP test. This was mimicked by intrathecal 6-OHDA which depleted NA in the spinal cord, but not by microinjection of 6-OHDA into the dorsal bundle which depleted NA in the forebrain. These results suggest an integral involvement of noradrenergic mechanisms in the antinociceptive action of caffeine in the HP and formalin tests and in locomotor stimulation, but the nature of this involvement differs for the 3 end points.

Adrenergic alpha-Antagonists↗
PubMed1993

Caffeine depression of spontaneous activity in rabbit sino-atrial node cells.

1. Effects of caffeine on the action potentials and the membrane currents in spontaneously beating rabbit sino-atrial (SA) node cells were examined using a two-microelectrode technique. 2. Cumulative administrations of caffeine (1-10 mM) caused a negative chronotropic effect in a concentration-dependent manner, which was not modified by atropine (0.1 microM). At 10 mM, caffeine increased the amplitude and prolonged the duration of action potentials significantly; the other parameters were unaffected. 3. In 3 of 16 preparations, caffeine (5 mM) elicited arrhythmia. At high Ca2+ (8.1 mM), caffeine (5 mM) increased the incidence of arrhythmia. 4. Caffeine (0.5-10 mM) enhanced the slow inward current, but at 10 mM decreased the enhanced peak current by 5 mM. The hyperpolarization-activated inward current was also enhanced by caffeine, but 10 mM caffeine decreased the current peak as compared with that at 5 mM. In addition, caffeine inhibited the delayed rectifying outward current in a concentration-dependent manner, accompanied by a depressed activation curve without any shift in the half-maximum activation voltage. 5. Caffeine elevated the cytoplasmic Ca2+ level in the SA node cells loaded with Ca(2+)-sensitive fluorescent dye (fura-2). 6. These results suggest that caffeine enhances and/or inhibits the ionic currents and elicits arrhythmia due to the induction of cellular calcium overload.

Action Potentials↗
PubMed1991

The effects of caffeine on ischemic neuronal injury as determined by magnetic resonance imaging and histopathology.

The effects of caffeine on ischemic neuronal injury were determined in rats subjected to forebrain ischemia induced by bilateral carotid occlusion and controlled hypotension (50 mmHg for 10 min). High resolution (100 microns) multi-slice, multi-echo magnetic resonance images were obtained daily for three consecutive days post-operatively in sham-operated rats and in rats that received either saline vehicle (controls), a single i.v. injection of 10 mg/kg caffeine 30 min prior to an ischemic insult (acute caffeine group), or up to 90 mg/kg per day of caffeine for three consecutive weeks prior to an ischemic insult (chronic caffeine group). Rats in the control group exhibited enhanced magnetic resonance image intensity in the striatum 24 h after ischemia which increased in the striatum and also appeared in the hippocampus after 48 h, and which began to resolve in both regions by 72 h post-ischemia. Histopathological analysis of each rat following the final magnetic resonance examination showed that ischemic neuronal injury was strictly confined to the brain regions showing magnetic resonance image changes. Acute caffeine rats showed accelerated changes in the magnetic resonance images, with increased hippocampal intensity appearing at 24 h post-ischemia. Although there was magnetic resonance evidence of accelerated injury, quantitative analysis of the histopathological data at 72 h showed no significant difference in the extent of neuronal injury in any brain region between control-ischemic and acute caffeine rats. Nine out of 11 rats in the chronic caffeine group showed no magnetic resonance image changes over the three study days. Chronic caffeine rats had significantly less neuronal damage in all vulnerable brain regions than either of the other groups of ischemic rats. The accelerated ischemic injury in rats treated with an acute dose of caffeine may occur secondary to antagonism of adenosine receptors, whereas protection from ischemic injury following chronic administration of caffeine may be mediated by up-regulation of adenosine receptors.

Adenosine↗
PubMed1995

Caffeine elevates blood pressure response to exercise in mild hypertensive men.

The present study examined the effects of caffeine on blood pressure (BP) regulation in hypertensive men during exercise. Twenty unmedicated, mild hypertensives (HT, BP = 140/90 to 160/105 mm Hg) and 12 age-matched, normotensives (NT, BP < 130/80 mm Hg) performed 30 min of extended bicycle exercise following a single dose of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) and placebo in a double-blind, cross-over design. Hemodynamic measurements were made at predrug, 40-min postdrug and during exercise. At predrug baseline, HT had significantly higher HR (67 v 57 beats/min) and BP (141/96 v 118/72 mm Hg) than NT. At postdrug baseline, caffeine increased systolic and diastolic BP, and peripheral vascular resistance (P < .01 in all cases), decreased HR (P < .05) and did not significantly change stroke volume and cardiac output for both groups. During exercise, HR response was greater on caffeine day than placebo day in HT (P < 0.05) only. Systolic BP was consistently elevated on caffeine day compared to placebo day in both groups (P < .001). Diastolic BP was elevated in HT for 30 min of exercise on caffeine day, but this pressor effect disappeared at 15 min of exercise in NT. As a result, rate-pressure products were significantly higher on caffeine days in HT at postdrug and during exercise. On caffeine day, 7 (39%) HT and 1 (8%) NT showed an excessive BP response (> 230 for systolic or > 120 for diastolic) during exercise. In conclusion, caffeine has significant hemodynamic effects on mild hypertensives at rest and during exercise. The increased rate-pressure products following caffeine during exercise place a greater workload on the heart, and abstinence from caffeine, especially before exercise, may be beneficial for persons with hypertension.

Adult↗
PubMed1994

Ca2+ mobilization by caffeine in single smooth muscle cells of the rat tail artery.

The fluorescent dye fura-2 was used to study the effects of caffeine on cytosolic free Ca2+ level ([Ca2+]i) in freshly isolated single cells from the rat tail artery. Caffeine caused a concentration-dependent transient increase in [Ca2+]i and shortening of the cell. At higher concentrations (> 2 mM), a tonic increase in [Ca2+]i was also observed. The caffeine-induced changes in [Ca2+]i were reproducible with repeated challenges, even though the cells had contracted due to previous exposure to caffeine. Removal of extracellular Ca2+ reduced the resting [Ca2+]i to about half and abolished the tonic Ca2+ increase to caffeine. The transient component was not significantly affected to the first caffeine challenge after Ca2+ removal, but was abolished to the second challenge. Ryanodine (10 microM) significantly inhibited the responses to caffeine while nifedipine and TMB-8-(8-(diethylamino)octyl ester of 3,4,5-trimethoxybenzoic acid) were not effective. Thapsigargin (10-100 microM) induced a sustained increase in [Ca2+]i to 67 nM. The response of caffeine was not affected by thapsigargin. Pretreatment of the cells with noradrenaline (10 microM) abolished subsequent response to caffeine. These results show that Ca2+ responses to caffeine in single cells from the rat tail artery are reproducible with repeated caffeine challenge. Therefore, single cells can be used for comparison studies of the effects of pharmacological agents.

Animals↗
PubMed2005

Association of ambulatory blood pressure and dietary caffeine in adolescents.

BACKGROUND: Although relatively little is known about the responsible factors, there is an increased prevalence of essential hypertension in youth. Our previous research using casual blood pressure (BP) suggests a role for caffeine intake. The objective of this study was to assess the association between caffeine intake and ambulatory BP patterns among adolescents and to replicate our previous findings that compared caffeine intake to BP values obtained at a single time point. METHODS: Eighty-two African-American and non-Hispanic white adolescents (15 to 19 years old) with normal systolic BP selected foods and beverages for a 4-day sodium-controlled diet. Subjects were stratified into three groups based on the amount of caffeine in these foods. Ambulatory BP measures (24-h) were recorded during 1 day of the 4-day diet. The effects of ethnicity, caffeine, and the interaction of ethnicity and caffeine on BP were assessed for daytime and nighttime hours controlling for gender and body mass index. RESULTS: The level of dietary caffeine was positively associated with daytime systolic BP (F(2,76) = 3.1, P = .05, partial R(2) = 0.07) and daytime diastolic BP (F = 3.53(2,76), P = .03, partial R(2) = 0.07). Caffeine's effect on systolic BP was most pronounced for African-American subjects. These results replicated our earlier findings. There was no association between caffeine intake and nighttime BP. CONCLUSIONS: This investigation replicates and extends our previous findings that caffeine consumption impacts the BP of adolescents, during the daytime when sympathetic nervous system responses dominate BP control. Controlled studies that examine the pressor effects of caffeine intake at levels typical of the dietary patterns of today's adolescents are needed.

Adolescent↗
PubMed2005

Caffeine metabolism, genetics, and perinatal outcomes: a review of exposure assessment considerations during pregnancy.

PURPOSE: To review the methodologic issues complicating caffeine exposure assessment during pregnancy; to discuss maternal and fetal caffeine metabolism, including genetic polymorphisms affecting caffeine metabolism; and to discuss the endogenous and exogenous risk factors known to influence caffeine metabolism. METHODS: A review of the relevant literature. RESULTS: There is wide inter-individual variation in caffeine metabolism, primarily due to variations in CYP1A2 enzyme activity. Some variability in CYP1A2 activity is due to genetic polymorphisms in the CYP1A2 gene which can cause increased or decreased inducibility of the enzyme. Considerable evidence exists that maternal caffeine metabolism is influenced by a variety of endogenous and exogenous factors and studying the genetic polymorphisms may improve understanding of the potential effects of caffeine and its metabolites on perinatal outcomes. There is substantial evidence that measurement of maternal, fetal, and neonatal caffeine metabolites may allow for a more precise measure of fetal caffeine exposure. CONCLUSIONS: Research on the genetic polymorphisms affecting caffeine metabolism may further explain the potential effects of caffeine and its metabolites on perinatal outcomes.

Caffeine↗