Aldosterone and postprandial renal excretion of sodium and potassium in sheep

Rabinowitz, L.; Denham, Simon; Gunther, R. A.

doi:10.1152/ajprenal.1977.233.3.f213

Cited by 14 publications

(13 citation statements)

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“…Regardless, the literature is dominated by the study of natriuretic influences following a meal. The ability to eliminate an acute salt load has been attributed to many factors, such as withdrawal of the renin-angiotensinaldosterone system (5,36), increased natriuretic peptide (12,39,46), withdrawal of renal sympathetic nerve activity (32,35), hemodynamic factors (20), and gut-derived hormones such as glucagon-like peptide (GLP-1; Ref. 17), amylin, secretin, vasoactive intestinal peptide, glucagon, and uroguanylin (14,30,45).…”

Section: Perspectives and Significancementioning

confidence: 99%

The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses

Irsik

Blazer‐Yost

Staruschenko

et al. 2017

American Journal of Physiology-Regulatory, Integrative and Comp

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Despite the effects of insulinopenia in type 1 diabetes and evidence that insulin stimulates multiple renal sodium transporters, it is not known whether normal variation in plasma insulin regulates sodium homeostasis physiologically. This study tested whether the normal postprandial increase in plasma insulin significantly attenuates renal sodium and volume losses. Rats were instrumented with chronic artery and vein catheters, housed in metabolic cages, and connected to hydraulic swivels. Measurements of urine volume and sodium excretion (UNaV) over 24 h and the 4-h postprandial period were made in control (C) rats and insulin-clamped (IC) rats in which the postprandial increase in insulin was prevented. Twenty-four-hour urine volume (36 ± 3 vs. 15 ± 2 ml/day) and UNaV (3.0 ± 0.2 vs. 2.5 ± 0.2 mmol/day) were greater in the IC compared with C rats, respectively. Four hours after rats were given a gel meal, blood glucose and urine volume were greater in IC rats, but UNaV decreased. To simulate a meal while controlling blood glucose, C and IC rats received a glucose bolus that yielded peak increases in blood glucose that were not different between groups. Urine volume (9.7 ± 0.7 vs. 6.0 ± 0.8 ml/4 h) and UNaV (0.50 ± 0.08 vs. 0.20 ± 0.06 mmol/4 h) were greater in the IC vs. C rats, respectively, over the 4-h test. These data demonstrate that the normal increase in circulating insulin in response to hyperglycemia may be required to prevent excessive renal sodium and volume losses and suggest that insulin may be a physiological regulator of sodium balance.

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Section: Perspectives and Significancementioning

confidence: 99%

The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses

Irsik

Blazer‐Yost

Staruschenko

et al. 2017

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Physiologists studying potassium homeostasis were surprised to discover that even minor changes in dietary potassium intake, insufficient to change plasma concentrations of either potassium (23) or aldosterone (24) and therefore too minor to activate feedback control, evoked rapid changes in renal potassium excretion through feedforward mechanisms. Twenty-five years ago, Rabinowitz and colleagues (25) challenged feedback regulation as the sole mechanism for compensatory renal potassium excretion and proposed a feedforward kaliuretic reflex, in which potassium sensors in the splanchnic vascular bed (the gut, portal vein, or liver) detect local changes in potassium concentration resulting from potassium ingestion and signal the kidney to alter potassium excretion to restore balance (Figure 1).…”

Section: Feedforward Control Of Potassium Balancementioning

confidence: 99%

Narrative Review: Evolving Concepts in Potassium Homeostasis and Hypokalemia

et al. 2009

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Humans are intermittently exposed to large variations in potassium intake, which range from periods of fasting to ingestion of potassium-rich meals. These fluctuations would abruptly alter plasma potassium concentration if not for rapid mechanisms, primarily in skeletal muscle and the liver, that buffer the changes in plasma potassium concentration by means of transcellular potassium redistribution and feedback control of renal potassium excretion. However, buffers have capacity limits, and even robust feedback control mechanisms require that the perturbation occur before feedback can initiate corrective action. In contrast, feedforward control mechanisms sense the effect of disturbances on the system’s homeostasis. This review highlights recent experimental insights into the participation of feedback and feedforward control mechanisms in potassium homeostasis. New data make clear that feedforward homeostatic responses activate when decreased potassium intake is sensed, even when plasma potassium concentration is still within the normal range and before frank hypokalemia ensues, in addition to the classic feedback activation of renal potassium conservation when plasma potassium concentration decreases. Given the clinical importance of dyskalemias in patients, these novel experimental paradigms invite renewed clinical inquiry into this important area.

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“…It has been suggested that the postprandial natriuresis is mediated by a decrease in plasma renin and hence aldosterone levels (Rabinowitz et al . 1977).…”

Section: Discussionmentioning

confidence: 99%

Influence of ruminal water‐loading on renal sodium excretion and water intake following feeding in sheep

Mathai

Thomson

2001

Acta Physiologica Scandinavica

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We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 +/- 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L (-1) and plasma osmolality by 9 mosmol kg (-1) within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water-loaded animals compared with untreated animals (30.4 +/- 2.1 mmol (-1) cf. 63.8 +/- 2.9 mmol-1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.

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Aldosterone and postprandial renal excretion of sodium and potassium in sheep

Cited by 14 publications

References 0 publications

The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses

The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses

Narrative Review: Evolving Concepts in Potassium Homeostasis and Hypokalemia

Influence of ruminal water‐loading on renal sodium excretion and water intake following feeding in sheep

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