scholarly journals Increased oral sodium chloride intake in humans amplifies selectively postprandial GLP‐1 but not GIP, CCK, and gastrin in plasma

2020 ◽  
Vol 8 (15) ◽  
Author(s):  
Ali Asmar ◽  
Per K. Cramon ◽  
Meena Asmar ◽  
Lene Simonsen ◽  
Charlotte M. Sorensen ◽  
...  
Keyword(s):  
Sodium Chloride ◽  
Sodium Chloride Intake ◽  
Oral Sodium

scholarly journals Stabilization of the Serum Lithium Concentration by Regulation of Sodium Chloride Intake: Case Report

2016 ◽  
Vol 136 (3) ◽  
pp. 517-521 ◽  
Author(s):  
Takashi Tomita ◽  
Hidekazu Goto ◽  
Kenji Sumiya ◽  
Tadashi Yoshida ◽  
Katsuya Tanaka ◽  
...  
Keyword(s):  
Case Report ◽  
Sodium Chloride ◽  
Lithium Concentration ◽  
Serum Lithium Concentration ◽  
Sodium Chloride Intake

Specific alterations in sodium chloride intake after hypothalamic lesions in the rat

1963 ◽  
Vol 205 (5) ◽  
pp. 922-926 ◽  
Author(s):  
Miguel R. Covian ◽  
José Antunes-Rodrigues
Keyword(s):  
Sodium Chloride ◽  
Urinary Excretion ◽  
The Other ◽  
Urinary Output ◽  
Water Ingestion ◽  
Hypothalamic Lesions ◽  
Paraventricular Nuclei ◽  
Electrolytic Lesions ◽  
Specific Increase ◽  
Sodium Chloride Intake

Bilateral electrolytic lesions in the hypothalamus of the rat elicited either a decrease or increase in 2% NaCl intake, without a significant change in water ingestion. Lesions placed in the anterior hypothalamus involving supraoptic or paraventricular nuclei, or both, resulted in a conspicuous fall (as much as 93%) of NaCl intake. The decreased consumption remained to the end of the experiments which in some rats lasted 105 days and was accompanied by a decrease in NaCl urinary output. On the contrary, lesions placed in the central hypothalamus determined a specific increase of NaCl intake together with an augmented urinary excretion. The increased ingestion was permanent and lasted to the end of the experiment, attaining in one rat the value of 290%. To account for these results two provisional explanations are advanced, one of them considering the possibility of the existence of two areas of opposite effects regarding NaCl ingestion and the other claiming a neurohumoral mechanism in which oxytocin and aldosterone could be the two responsible hormones.

Effect of dietary potassium chloride in borderline hypertensive rats.

1992 ◽  
Vol 3 (2) ◽  
pp. 188-195
Author(s):  
G F DiBona ◽  
S Y Jones
Keyword(s):  
Sodium Chloride ◽  
Environmental Stress ◽  
Potassium Chloride ◽  
Spontaneously Hypertensive Rat ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Dietary Potassium ◽  
Sodium Chloride Intake

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.

P102 Sodium chloride intake in Isfahan population

1998 ◽  
Vol 136 ◽  
pp. S74
Author(s):  
M. Boshtam ◽  
M. Rafie ◽  
N. Sarrafzadegan ◽  
Gh. Naderi ◽  
S.Asgary Isfahan
Keyword(s):  
Sodium Chloride ◽  
Sodium Chloride Intake

Delayed Onset and Reduced Severity of Adrenal-Compression Hypertension in Rats Treated with Digitoxin

1976 ◽  
Vol 51 (s3) ◽  
pp. 159s-162s
Author(s):  
C. E. Hall ◽  
S. Ayachi ◽  
O. Hall
Keyword(s):  
Sodium Chloride ◽  
Cardiac Hypertrophy ◽  
Adrenal Glands ◽  
Severe Hypertension ◽  
Unilateral Nephrectomy ◽  
High Sodium ◽  
Delayed Onset ◽  
Sodium Chloride Intake

1. Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis. 2. Digitoxin treatment delayed the onset, reduced the incidence and ameliorated the magnitude of the hypertensive response in such rats; it also reduced the degree of cardiac hypertrophy, the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys or atrophy of the thymus.

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