Abstract
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.
Highlights
Excess dietary salt induces adverse cardiovascular and renal effects according to epidemiological, interventional, and experimental studies [1,2,3]
We prospectively examined the effects of salt and potassium supplementation on serum gastrin levels in normotensive and mildly hypertensive subjects
TheThe results of the present study demonstrate increasesserum serumgastrin gastrinlevels levels results of the present study demonstratethat thathigh highsalt salt intake intake increases fromfrom the the levels of the relatively low-salt diet
Summary
Excess dietary salt induces adverse cardiovascular and renal effects according to epidemiological, interventional, and experimental studies [1,2,3]. A peptide hormone secreted primarily by G-cells in response to food ingestion, is released into the blood stream. It is the principal mediator of meal-induced gastric phase and acid secretion and acts via paracrine stimulation of histamine released from gastric enterochromaffin-like cells [9,10,11]. Gastrin acts on its receptor, cholecystokinin B receptor (CCKBR), to regulate gastric acid secretion and oxyntic gland proliferation and exert physiological actions outside the gastric mucosa, in the colon, pancreas, small intestine, liver, esophagus, and kidney [12]. CCKBR is widely expressed in the kidney, especially in the glomerular mesangial cells, collecting duct cells, Nutrients 2017, 9, 389; doi:10.3390/nu9040389 www.mdpi.com/journal/nutrients
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