A High-Salt Meal Produces Natriuresis in Humans Without Elevating Plasma Atriopeptin

Saville, Mark A.; Geer, P. G.; Wang, Bin C.; Leadley, Robert J.; Goetz, K. L.

doi:10.3181/00379727-188-3-rc2

Cited by 17 publications

(14 citation statements)

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“…Our conclusion is further strengthened by the selection of intermeal intervals, between treatment consumption and the measurement of FI and WI, that spanned the times for which acute effects of Na + intake have been reported (Hunt and Pathak 1960;Driver 1988;Saville et al 1988). FI was measured 120 min after treatment consumption in experiment 1 for two reasons.…”

Section: Discussionmentioning

confidence: 95%

“…In a previous study of healthy adults, ingestion of 2300 mg Na + dissolved in water increased plasma osmolality to the thirst threshold within 30 min (Saville et al 1988), a change that triggers WI (Vokes 1987). On each of the 5 treatment days, participants consumed 1 of 5 tomato beverages, which had 0, 500, 1000, 1500, or 2000 mg of added Na + .…”

Section: Methodsmentioning

confidence: 96%

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Acute sodium ingestion has no effect on short-term food and water intake, subjective appetite, thirst, or glycemic response in healthy young men

Nunez

Mollard

Luhovyy

et al. 2013

Appl. Physiol. Nutr. Metab.

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The high intake of dietary sodium (Na(+)) has been associated with obesity and insulin resistance, sparking the hypothesis that the consumption of salty foods affects food intake (FI) and postprandial blood glucose (BG) response. Therefore, we conducted 2 randomized repeated-measures experiments to examine the acute effects of the Na(+) content of solid food and beverage on FI, water intake (WI), subjective appetite, thirst, and BG. FI and WI were measured at ad libitum pizza test meals; appetite, thirst, and BG were measured at baseline and at regular intervals before and after meals. In the first experiment, 16 males (mean body mass index (BMI), 22.2 kg·m(-2)) consumed a low-Na(+) (71 mg) bean preload (300 kcal) with or without 740 mg or 1480 mg of added Na(+) 120 min prior to the pizza meal. Participants ate 116 kcal more at the test meal after consuming beans with 740 mg of added Na(+) than after beans with 1480 mg of added Na(+). In the second experiment, 19 males (mean BMI, 23.2 kg·m(-2)) consumed a low-Na(+) (62 mg) tomato beverage (73 kcal) with or without 500, 1000, 1500, or 2000 mg of added Na(+) 30 min prior to a pizza meal. The beverage with 2000 mg of added Na(+) led to higher WI during the pizza meal than the beverage with 500 mg of added Na(+). However, compared with the control conditions (no added Na(+)), added Na(+) treatments had no effect on dependent measures in either experiment. In conclusion, the acute intake of Na(+), in a solid or liquid form, did not affect short-term subjective ratings of appetite or thirst, ad libitum FI or WI, or BG in healthy young men.

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Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 96%

Acute sodium ingestion has no effect on short-term food and water intake, subjective appetite, thirst, or glycemic response in healthy young men

Nunez

Mollard

Luhovyy

et al. 2013

Appl. Physiol. Nutr. Metab.

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“…The measurement of plasma atriopeptin only once each day would be unlikely to detect changes in this hormone that might occur transiently after sodium ingestion. Saville and his coworkers 21 attempted to detect postprandial changes by measuring circulating atriopeptin before and after normal human subjects ate a high sodium breakfast containing 100 mmol sodium chloride. On a separate morning several weeks later, the subjects ate a low sodium breakfast that contained the same number of calories but only 4 mmol sodium chloride.…”

Section: Alterations In Dietary Sodiummentioning

confidence: 99%

“…The key observation, however, was that plasma atriopeptin did not increase after either meal. Saville and his colleagues 21 concluded that atriopeptin was not responsible for the natriuresis induced by the high salt meal or for the diuresis induced by the low salt meal.…”

Section: Alterations In Dietary Sodiummentioning

confidence: 99%

Evidence that atriopeptin is not a physiological regulator of sodium excretion.

Goetz

1990

Hypertension

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Although much experimental evidence is consistent with the concept that atrial natriuretic factor (atriopeptin) is an important physiological regulator of renal sodium excretion, this hypothesis remains unproven. Indeed, a rapidly expanding collection of experimental data appears to be more compatible with the opposite conclusion, namely that circulating atriopeptin exerts only a trivial effect on renal sodium excretion during normal day-to-day living conditions. In this review, the substantial evidence demonstrating that elevations of plasma atriopeptin from threefold to 13-fold produce only a slowly developing and relatively modest natriuresis is reassessed in light of recently published data indicating that the acute intake of food (the pathway by which essentially all sodium enters the body under normal living conditions) does not increase circulating atriopeptin. These considerations imply that atriopeptin does not contribute to the process that elicits a postprandial natriuresis, a process that presumably is of primary importance in the physiological regulation of sodium balance. In addition, consideration is given to a number of common physiological, experimental, and pathophysiological conditions in which circulating atriopeptin does not correlate with renal sodium excretion. This lack of correlation implies that atriopeptin is not an important regulator of sodium excretion in these situations. (Hypertension 1990;15:9-19) T he widespread belief that atrial natriuretic factor (atriopeptin) plays an important role in the homeostatic regulation of renal sodium excretion appears to have developed largely because of three factors. The factors, not necessarily in order of importance, are: 1) extensive use of the term atrial natriuretic factor, a designation that implies that this hormone plays a primary role in the regulation of sodium excretion; 2) evidence demonstrating that infusion of this peptide into experimental animals and human subjects elicits a natriuresis; and 3) evidence demonstrating that certain stimuli cause both an increase in circulating atrial peptide and an increase in renal sodium excretion.The evidence mentioned above is well documented in scores of papers. Indeed, it is doubtful that anyone would attempt to refute the abundant data indicating that elevations of plasma atriopeptin of severalfold are capable of inducing a natriuresis. In addition, it is well established that certain natriuretic stimuli (e.g., volume expansion or left atrial distension) evoke an elevation in circulating atriopeptin that may correlate temporally with the evoked rise in sodium excretion.

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“…In contrast, in chronic volume expansion, induced by high dietary sodium intake, no change or a minimum de gree o f increase in plasma A N P has been reported [78,79]. Also, a study using autoimmune rats against A N P demon strated that natriuresis produced by chronic oral salt load ing was comparable to that o f control animals [77], It appears, therefore, that A N P does not play a major role in the Huid homeostasis during chronic, as opposed to acute, volume expansion.…”

Section: Volume Expansionmentioning

confidence: 99%