ReviewExperimental physiology2016
The importance of the gastrorenal axis in the control of body sodium homeostasis.
Review in Experimental physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Randomized Crossover Trial of Low Sodium Dialysate on Tissue Sodium Accumulation in Hemodialysis.Kidney international reports · 2026Article
- Systematic-Narrative Hybrid Literature Review: Crosstalk between Gastrointestinal Renin-Angiotensin and Dopaminergic Systems in the Regulation of Intestinal Permeability by Tight Junctions.International journal of molecular sciences · 2024Review
- Gastrin attenuates sepsis-induced myocardial dysfunction by down-regulation of TLR4 expression in macrophages.Acta pharmaceutica Sinica. B · 2023Article
- Intestinal Gastrin/CCKBR (Cholecystokinin B Receptor) Ameliorates Salt-Sensitive Hypertension by Inhibiting Intestinal NaHypertension (Dallas, Tex. : 1979) · 2022Article
- Gastrin, via activation of PPARα, protects the kidney against hypertensive injury.Clinical science (London, England : 1979) · 2021Article
- Gastrin Attenuates Renal Ischemia/Reperfusion Injury by a PI3K/Akt/Bad-Mediated Anti-apoptosis Signaling.Frontiers in pharmacology · 2020Review
- Hypertension as a Metabolic Disorder and the Novel Role of the Gut.Current hypertension reports · 2019Review
- Noncoding RNAs in the Regulatory Network of Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Identification of Alkaloids fromMolecules (Basel, Switzerland) · 2018Article
- Article
- Gastrointestinal Tract: a Promising Target for the Management of Hypertension.Current hypertension reports · 2017Review
- Gastrointestinal-Renal Axis: Role in the Regulation of Blood Pressure.Journal of the American Heart Association · 2017Review
- The Renal Sodium Bicarbonate Cotransporter NBCe2: Is It a Major Contributor to Sodium and pH Homeostasis?Current hypertension reports · 2016Review
- Gastrorenal communication: sniffing and tasting.Experimental physiology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
NEW
findingsWhat is the topic of this review? Sensing the amount of ingested sodium is one mechanism by which sodium balance is regulated. This review describes the role of gastrin in the cross-talk between the stomach and the kidney following the ingestion of sodium. What advances does it highlight? Neural mechanisms and several gut hormones, including cholecystokinin and uroguanylin, have been suggested to mediate the natriuresis after an oral sodium load. It is proposed that gastrin produced by G-cells via its receptor, cholecystokinin B receptor, interacts with renal D1 -like dopamine receptors to increase renal sodium excretion. Hypertension develops with chronically increased sodium intake when sodium that accumulates in the body can no longer be sequestered, extracellular fluid volume is expanded, and compensatory neural, hormonal and pressure-natriuresis mechanisms fail. Sensing the amount of ingested sodium, by the stomach, is one mechanism by which sodium balance is regulated. The natriuresis following the ingestion of a certain amount of sodium may be due to an enterokine, gastrin, secreted by G-cells in the stomach and duodenum and released into the circulation. Circulating gastrin levels are 10- to 20-fold higher than those for cholecystokinin. Of all the gut hormones circulating in the plasma, gastrin is the one that is reabsorbed to the greatest extent by renal tubules. Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal sodium transport. Germline deletion of gastrin (Gast) or Cckbr gene in mice causes salt-sensitive hypertension. Selective silencing of Gast in the stomach and duodenum impairs the ability to excrete an oral sodium load and also increases blood pressure. Thus, the gastrorenal axis, mediated by gastrin, can complement pronatriuretic hormones, such as dopamine, to increase sodium excretion after an oral sodium load. These studies in mice may be translatable to humans because the chromosomal loci of CCKBR and GAST are linked to human essential hypertension. Understanding the role of genes in the regulation of renal function and blood pressure may lead to the tailoring of antihypertensive treatment based on genetic make-up.
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