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

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          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.

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          Most cited references26

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          Plasma sodium stiffens vascular endothelium and reduces nitric oxide release.

          Dietary salt plays a major role in the regulation of blood pressure, and the mineralocorticoid hormone aldosterone controls salt homeostasis and extracellular volume. Recent observations suggest that a small increase in plasma sodium concentration may contribute to the pressor response of dietary salt. Because endothelial cells are (i) sensitive to aldosterone, (ii) in physical contact with plasma sodium, and (iii) crucial regulators of vascular tone, we tested whether acute changes in plasma sodium concentration, within the physiological range, can alter the physical properties of endothelial cells. The tip of an atomic force microscope was used as a nanosensor to measure stiffness of living endothelial cells incubated for 3 days in a culture medium containing aldosterone at a physiological concentration (0.45 nM). Endothelial cell stiffness was unaffected by acute changes in sodium concentration <135 mM but rose steeply between 135 and 145 mM. The increase in stiffness occurred within minutes. Lack of aldosterone in the culture medium or treatment with the epithelial sodium channel inhibitor amiloride prevented this response. Nitric oxide formation was found down-regulated in cells cultured in aldosterone-containing high sodium medium. The results suggest that changes in plasma sodium concentration per se may affect endothelial function and thus control vascular tone.
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            Cholecystokinin and gastrin receptors.

            Cholecystokinin and gastrin receptors (CCK1R and CCK2R) are G protein-coupled receptors that have been the subject of intensive research in the last 10 years with corresponding advances in the understanding of their functioning and physiology. In this review, we first describe general properties of the receptors, such as the different signaling pathways used to exert short- and long-term effects and the structural data that explain their binding properties, activation, and regulation. We then focus on peripheral cholecystokinin receptors by describing their tissue distribution and physiological actions. Finally, pathophysiological peripheral actions of cholecystokinin receptors and their relevance in clinical disorders are reviewed.
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              GenSalt: rationale, design, methods and baseline characteristics of study participants.

              (2007)
              Hypertension is a complex disorder influenced by genetic and environmental determinants and their interactions. The objectives of the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) are to localize and identify genes related to blood pressure (BP) responses to dietary sodium and potassium intervention. GenSalt utilizes a family feeding-study design. Each family was ascertained through a proband with untreated prehypertension or stage-1 hypertension in rural China. A medical history, lifestyle risk factors and responses to cold pressor tests, were obtained at baseline visits while BP, weight, blood and urine specimens were collected at baseline and follow-up visits. The dietary intervention included a 7-day low-sodium feeding (51.3 mmol/day), a 7-day high-sodium feeding (307.8 mmol/day) and a 7-day high-sodium feeding with an oral potassium supplementation (60 mmol/day). Microsatellite markers for genome-wide linkage scan and single nucleotide polymorphism (SNP) markers in candidate genes will be genotyped. Overall, 3153 participants from 658 families were recruited for GenSalt. The mean systolic and diastolic BPs were 128.0 and 80.3, 111.6 and 71.0, 112.6 and 72.6, 106.6 and 65.3 and 136.7 and 75.0 mm Hg for probands, siblings, spouses, offspring and parents, respectively. The mean urinary excretion of sodium and potassium were 232.5 and 38.6, 222.9 and 38.2, 213.1 and 37.8 and 207.3 and 36.0 mmol/24-h for probands, siblings, spouses and offspring, respectively. Our study will identify novel genes that influence significantly the effect of dietary sodium and potassium intake on BP. This information is useful for development of targeted intervention for the prevention and treatment of hypertension.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                14 April 2017
                April 2017
                : 9
                : 4
                : 389
                Affiliations
                [1 ]Department of Physics, Harbin University, Harbin 150086, China; gongxlyc@ 123456hrbu.edu.cn
                [2 ]Cardio-Cerebrovascular Control and Research Center, Institute of Basic Medicine, Shandong Academy of Medical Sciences, Jinan 250062, China; hewenwenxxk@ 123456hrbu.edu.cn (W.-W.H.); linyf1990@ 123456hrbu.edu.cn (Y.-F.L.)
                Author notes
                [* ]Correspondence: wyy_janet@ 123456163.com (Y.-Y.W.); lufeihong@ 123456hrbu.edu.cn (L.-F.H.); Tel.: +86-451-8661-4321 (Y.-Y.W.); +86-451-5892-9025 (L.-F.H.)
                Article
                nutrients-09-00389
                10.3390/nu9040389
                5409728
                28420122
                830afbf4-eeb1-47ef-b512-d7dfa8b4cdd8
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 11 January 2017
                : 13 April 2017
                Categories
                Article

                Nutrition & Dietetics
                gastrin,salt,potassium,sodium excretion,blood pressure
                Nutrition & Dietetics
                gastrin, salt, potassium, sodium excretion, blood pressure

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