Novel Gastro-Renal Axis and Sodium Regulation During Hypertension

Banday, Anees Ahmad; Lokhandwala, Mustafa F.

doi:10.1161/hypertensionaha.113.01799

Cited by 6 publications

(6 citation statements)

References 9 publications

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“…In the past few years, several studies have suggested that gastrointestinal hormones are involved in the regulation of renal function (Von et al, 2000;Banday and Lokhandwala, 2013;Jose, 2016;Jose et al, 2016a;Jose et al, 2016b). Gastrin has been reported to interact with dopamine receptor to modulate the renal sodium excretion and thus participates in the regulation of blood pressure (Chen et al, 2013;Jiang et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Gastrin Attenuates Renal Ischemia/Reperfusion Injury by a PI3K/Akt/Bad-Mediated Anti-apoptosis Signaling

et al. 2020

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Ischemic/reperfusion (I/R) injury is the primary cause of acute kidney injury (AKI). Gastrin, a gastrointestinal hormone, is involved in the regulation of kidney function of sodium excretion. However, whether gastrin has an effect on kidney I/R injury is unknown. Here we show that cholecystokinin B receptor (CCKBR), the gastrin receptor, was significantly up-regulated in I/R-injured mouse kidneys. While pre-administration of gastrin ameliorated I/R-induced renal pathological damage, as reflected by the levels of serum creatinine and blood urea nitrogen, hematoxylin and eosin staining and periodic acid-Schiff staining. The protective effect could be ascribed to the reduced apoptosis for gastrin reduced tubular cell apoptosis both in vivo and in vitro. In vitro studies also showed gastrin preserved the viability of hypoxia/ reoxygenation (H/R)-treated human kidney 2 (HK-2) cells and reduced the lactate dehydrogenase release, which were blocked by CI-988, a specific CCKBR antagonist. Mechanistically, the PI3K/Akt/Bad pathway participates in the pathological process, because gastrin treatment increased phosphorylation of PI3K, Akt and Bad. While in the presence of wortmannin (1 μM), a PI3K inhibitor, the gastrin-induced phosphorylation of Akt after H/R treatment was blocked. Additionally, wortmannin and Akt inhibitor VIII blocked the protective effect of gastrin on viability of HK-2 cells subjected to H/R treatment. These studies reveals that gastrin attenuates kidney I/R injury via a PI3K/Akt/Bad-mediated anti-apoptosis signaling. Thus, gastrin can be considered as a promising drug candidate to prevent AKI.

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Section: Discussionmentioning

confidence: 99%

Gastrin Attenuates Renal Ischemia/Reperfusion Injury by a PI3K/Akt/Bad-Mediated Anti-apoptosis Signaling

et al. 2020

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“…The gut microbiota can influence the ability of enterochromaffin cells to produce serotonin, dopamine, and norepinephrine that can influence the behavior of the host, termed brain gut microbiome axis (72, 73) and renal function, termed gastrorenal reflex (74, 75). The absence of gut microbiota has been reported to increase anxiety-like behavior and decreased dopamine turnover in the frontal cortex, hippocampus, and striatum in response to acute stress in rats (76).…”

Section: Gut Microbiota and Gastrorenal Axismentioning

confidence: 99%

Gut microbiota in hypertension

José

Raj²

2015

Current Opinion in Nephrology and Hypertension

167

109

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Purpose of review Hypertension, which is present in about one quarter of the world’s population, is responsible for about 41% of the number one cause of death, cardiovascular disease. Not included in these statistics is the effect of sodium intake on blood pressure, even though an increase or a marked decrease in sodium intake can increase blood pressure. This review deals with the interaction of gut microbiota and the kidney with genetics and epigenetics in the regulation of blood pressure and salt sensitivity. Recent findings The abundance of the gut microbes, Firmicutes and Bacteroidetes, is associated with increased blood pressure in several models of hypertension, including the spontaneously hypertensive and Dahl salt-sensitive rats. Decreasing gut microbiota by antibiotics can increase or decrease blood pressure that is influenced by genotype. The biological function of probiotics may also be a consequence of epigenetic modification, related, in part, to microRNA. Products of the fermentation of nutrients by gut microbiota can influence blood pressure by regulating expenditure of energy, intestinal metabolism of catecholamines, and gastrointestinal and renal ion transport, and thus, salt sensitivity. Summary The beneficial or deleterious effects of gut microbiota on blood pressure is a consequence of several variables, including genetics, epigenetics, lifestyle, and intake of antibiotics. These variables may influence the ultimate level of blood pressure and control of hypertension.

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“…In the current study, we observed a negative correlation between serum gastrin concentration and BP levels in the three intervention periods. In addition, gastrin is important in salt sensitivity, as indicated by result of the investigation on Gast −/− mice, which are normotensive at a low Na + intake but become hypertensive at a normal or high Na + intake [34]. Determining the molecular mechanism and signaling molecules responsible for the effects of gastrin on salt sensitivity and hypertension could be of great interest.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Salt Intake and Potassium Supplementation on Serum Gastrin Levels in Chinese Adults: A Randomized Trial

Wang

Yan-chun

et al. 2017

Nutrients

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Excess dietary salt is strongly correlated with cardiovascular disease, morbidity, and mortality. Conversely, potassium likely elicits favorable effects against cardiovascular disorders. Gastrin, which is produced by the G-cells of the stomach and duodenum, can increase renal sodium excretion and regulate blood pressure by acting on the cholecystokinin B receptor. The aim of our study was to assess the effects of altered salt and potassium supplementation on serum gastrin levels in humans. A total of 44 subjects (38–65 years old) were selected from a rural community in northern China. All subjects were sequentially maintained on a relatively low-salt diet for 7 days (3.0 g/day of NaCl), a high-salt diet for 7 days (18.0 g/day of NaCl), and then a high-salt diet supplemented with potassium for another 7 days (18.0 g/day of NaCl + 4.5 g/day of KCl). The high-salt intake significantly increased serum gastrin levels (15.3 ± 0.3 vs. 17.6 ± 0.3 pmol/L). This phenomenon was alleviated through potassium supplementation (17.6 ± 0.3 vs. 16.5 ± 0.4 pmol/L). Further analyses revealed that serum gastrin was positively correlated with 24 h urinary sodium excretion (r = 0.476, p < 0.001). By contrast, gastrin level was negatively correlated with blood pressure in all dietary interventions (r = −0.188, p = 0.031). The present study indicated that variations in dietary salt and potassium supplementation affected the serum gastrin concentrations in the Chinese subjects.

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Novel Gastro-Renal Axis and Sodium Regulation During Hypertension

Cited by 6 publications

References 9 publications

Gastrin Attenuates Renal Ischemia/Reperfusion Injury by a PI3K/Akt/Bad-Mediated Anti-apoptosis Signaling

Gastrin Attenuates Renal Ischemia/Reperfusion Injury by a PI3K/Akt/Bad-Mediated Anti-apoptosis Signaling

Gut microbiota in hypertension

The Effect of Salt Intake and Potassium Supplementation on Serum Gastrin Levels in Chinese Adults: A Randomized Trial

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