Comparative stimulant and diuretic actions of caffeine and theobromine in man

Dorfman, Louis; Jarvik, Murray E.

doi:10.1002/cpt1970116869

Cited by 56 publications

(20 citation statements)

References 2 publications

(2 reference statements)

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“…Administered acutely, caffeine is a diuretic. 26 One possibility is that caffeine-induced sodium depletion caused renal vasoconstriction and decreased responsiveness to Ang II. The similar serum sodium levels, urinary sodium excretion, and weight in the presence and absence of caffeine do not support this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Caffeine attenuates the renal vascular response to angiotensin II infusion.

1993

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Non-modulation has been proposed as an intermediate phenotype in human essential hypertension. The trait is characterized by blunted aldosterone and renal plasma flow responses to short-term angiotensin II (Ang II) infusion. Elevated tissue Ang II levels or decreased tissue adenosine levels could account for this decreased sensitivity to Ang II. In support of the latter possibility, endogenous adenosine has been shown to contribute to the renal vasoconstrictive response to Ang II in animals. We therefore tested the hypothesis that endogenous adenosine contributes to modulation of renal plasma flow in sodium-replete humans. We examined the effect of long-term administration of the adenosine receptor antagonist caffeine on baseline renal plasma flow and on the renal plasma flow response to short-term Ang II infusion in six salt-replete normotensive subjects in a single-blind, placebo-controlled study. para-Aminohlppurate clearance was used to assess renal plasma flow. Ang II was infused in graded doses (03 to 3 ng/kg per minute) in the presence and absence of caffeine (250 mg PO TID for 7 days). Blood pressure, plasma renin activity, Ang II, electrolytes, and pora-aminohippurate clearance were measured before and after each dose of Ang II. Caffeine did not alter either baseline blood pressure or the blood pressure response to Ang II but did increase baseline plasma renin activity from 0.72±0.09 to 1.42±0.26 ng angiotensin I/mL per hour (P=.01). Caffeine decreased the baseline renal plasma flow from 553±38 to 476±31 mL/min per 1.73 m 1 (P=.OO4) and attenuated the renal plasma flow response to a 3 ng/kg per minute infusion of Ang II (-106.5±25.2 versus -170.5±18 mL/min per 1.73 m 2 , P=.0O6). These data demonstrate that caffeine modulates baseline renal plasma flow and the renal plasma flow response to exogenous Ang II and therefore support the hypothesis that adenosine contributes to modulation of renal plasma flow in salt-replete humans. Thus, non-modulation may be partially acquired, and caffeine consumption must be controlled in studies that define modulation phenotype. (Hypertension. 1993;22:847-852.)

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Section: Discussionmentioning

confidence: 99%

Caffeine attenuates the renal vascular response to angiotensin II infusion.

1993

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“…Although these figures are below the 1-to 2-mg/kg single-dose intake associated with sleep distur bances in adults [Goldstein, 1964;Karacan et al, 1976;Dorfman and Jarvik, 1970], delayed excretion of caffeine by some infants could result in accumulation of pharmacologically significant amounts of caffeine.…”

Section: Discussionmentioning

confidence: 99%

Caffeine in Human Milk and in Serum of Breast-Fed Infants

Ryu¹

1985

Dev Pharmacol Ther

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A study was carried out to determine the caffeine concentration in milk of lactating women ingesting known amounts of caffeine and to determine serum concentration of caffeine of their infants. 9 lactating women and their infants were studied for 9 days. For the first 5 days, the women ingested 750 mg of caffeine daily, and for the next 4 days they ingested no caffeine and avoided coffee and other caffeine-containing products. The concentration of caffeine in samples of milk obtained by pooling aliquots from each feeding on day 5 averaged 4.3 µg/ml for 7 mothers who were 11-22 days after delivery on the 1st day of study. Values ranged from nondetectable (<0.25 µg/ml) to 15.7 pg/ml. No caffeine was detected in milk samples obtained on day 9. The mean concentration of caffeine in sera of the infants on day 5 was 1.4 µg/ml (range: nondetectable to 2.8 µg/ml). Caffeine was still detectable in 2 infants’ sera obtained on day 9. Concentrations had decreased only slightly since day 5. 2 older infants and their mothers were studied as described except that on days 5 and 9 samples of milk were obtained from each feeding and analyzed individually. The average caffeine concentrations in milk consumed on day 5 were 13.4 and 28.6 pg/ml, respectively. The concentrations of caffeine in infants’ sera on day 5 were <0.25 and 3.2 µg/ml. On day 9 milk and serum caffeine levels were below the limits of detectability.

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“…On the other hand there are no published data indicating that caffeine would not have the same sleep-depriving effect in children and adolescents as in adults. In adults, doses less than 100 mg, equivalent to 1.4 mg/kg bw, do not seem to have effect (Dorfman & Jarvik 1970).…”

Section: Short Summary Of Sleep Disturbancementioning

confidence: 89%