Sodium chloride intake of adrenalectomized rats with lateral hypothalamic lesions

1967 ◽  
Vol 212 (1) ◽  
pp. 113-118 ◽  
Author(s):  
G Wolf ◽  
D Quartermain
Keyword(s):  
Sodium Chloride ◽  
Hypothalamic Lesions ◽  
Lateral Hypothalamic ◽  
Sodium Chloride Intake ◽  
Adrenalectomized Rats

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.

Sodium Chloride Intake and Urinary Histamine in Adrenalectomized Rats

Nature ◽  
1959 ◽  
Vol 184 (4694) ◽  
pp. 1241-1241 ◽  
Author(s):  
T. BJURÖ ◽  
H. WESTLING
Keyword(s):  
Sodium Chloride ◽  
Urinary Histamine ◽  
Sodium Chloride Intake ◽  
Adrenalectomized Rats

Mechanism of decreased sodium chloride intake after hypothalamic lesions: Effect of hydrochlorothiazide

1970 ◽  
Vol 5 (10) ◽  
pp. 1183-1185 ◽  
Author(s):  
José Antunes-Rodrigues ◽  
Wilson A. Saad ◽  
Cleber G. Gentil ◽  
Miguel R. Covian
Keyword(s):  
Sodium Chloride ◽  
Hypothalamic Lesions ◽  
Sodium Chloride Intake

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

Microspectrofluorometric characterization of amine accumulation proximal to lateral hypothalamic lesions

1985 ◽  
Vol 334 (2) ◽  
pp. 344-347 ◽  
Author(s):  
Gregory L. Willis ◽  
Nigel G.M. Wreford ◽  
Graeme C. Smith
Keyword(s):  
Hypothalamic Lesions ◽  
Lateral Hypothalamic

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.

Sign in / Sign up

Export Citation Format

Share Document