The influence of foodstuffs on the rate of urinary acid excretion

Abstract

BRUNTON and ISRAELS [1930] noted that a rise of alveolar CO2 after mixed meals, first described by Dodds [1921], occurs more regularly than any such rise of alveolar CO2 after stimulation of gastric secretion by such agents as histamine or caffeine. They described experiments with these bases in which the (minimum) volumes of gastric secretion and the associated changes in the secretion of acid by the kidney were measured but in which no rise of alveolar C02 occurred. Dodds's subjects had usually taken mixed meals [Dodds, 1921;Dodds and Bennett, 1921;Bennett and Dodds, 1921;Dodds, 1923]. Moreover, in the various contributions to the solution of the question whether there is an " alkaline tide" after meals, too little attention has been paid to the composition of the meals, and it seemed possible that the conflicting results reported might be due to differences in the nature of the food taken by the subjects of the experiments. In any case it was desirable that information should be obtained as to the effects which specified articles of diet might have. Experiments are reported here as to the effect of various articles of diet upon the acidity of the urine and as controls for comparison other experiments in which nothing was taken, or merely water.Various methods have been used for studying the effect of meals on the acidity of the urine. The method adopted here involves a principle recognized by Do d ds, namely that the amount of urine passed in unit time should be combined with the titration equivalent of unit volume of the urine, and that the amount of titratable acid in the urine excreted in unit time so obtained is more significant than the amount in unit volume of urine. In the experiments to be described this principle is adhered to and the results are presented as curves showing the amount of titratable acid in the urine passed per minute. This may, for convenience, be referred to as "acid per minute," and the more usually estimated PH. LXXVIII. 5

The alkaline tide and ammonia excretion after voluntary feeding in freshwater rainbow trout

“…Several studies in humans have failed to see alkaline urine and respiratory compensation following feeding (e.g. Brunton, 1933;Johnson et al, 1995). These authors have even suggested that any respiratory or urinary compensation for gastric acid secretion is too small to be of physiological or clinical significance.…”

“…Perry et al, 2003;Evans et al, 2005;Tresguerres et al, 2006) and the restoration of resting blood acid-base chemistry likely reflects the ability of branchial base excretion mechanisms to adequately compensate for the metabolic alkalosis created during digestion, as in the elasmobranch Squalus acanthias (Wood et al, 2005;Wood et al, 2007a;Wood et al, 2007b;Tresguerres et al, 2007). The alkaline tide, at least for mammals, is also accompanied by excretion of alkaline urine (Rune, 1965;Rune 1966;Niv and Fraser, 2002) resulting from a reduction in the metabolic acid load normally excreted in the urine (Brunton, 1933). In fact, Finke and Litsenberger (Finke and Litsenberger, 1992) determined that postprandial pH of urine produced by cats was linearly correlated with meal size.…”

The molecular mechanism of CFTR‐ and secretin‐dependent renal bicarbonate excretion

“…During digestion, large amounts of acid are secreted from parietal cells into the stomach, causing a transient systemic alkalosis. This post-prandial plasma alkalinity is followed by a sharp reduction in net renal acid excretion and an increase in urinary pH (Brunton, 1933). It received the term the 'alkaline tide' , which describes the transient alkalinity of the urine after each meal that was discovered already in 1845 (Jones, 1845).…”

Alkalosis-induced hypoventilation in cystic fibrosis: The importance of efficient renal adaptation

“…The purpose of the alkaline tide, a long-known normophysiological process, has remained unresolved. The alkaline tide describes the acute rise in urine pH observed in the postprandial state ( 20 , 21 ) that attends the alkalinization of plasma pH when gastric acid secretion is stimulated upon ingestion of a meal. Recent evidence suggests urine pH and base excretion increase via a secretin-mediated pendrin- and CFTR-dependent increase of β-intercalated cell HCO 3 − secretion in the collecting ducts of the kidney ( 8 ).…”