scholarly journals Distribution of renin activity and angiotensinogen in rat brain. Effects of dietary sodium chloride intake on brain renin.

1985 ◽  
Vol 76 (5) ◽  
pp. 1939-1945 ◽  
Author(s):  
C P Genain ◽  
G R Van Loon ◽  
T A Kotchen
1989 ◽  
Vol 7 (11) ◽  
pp. 861-863 ◽  
Author(s):  
Christopher C. J. Miller ◽  
Nilesh J. Samani ◽  
Andrew T. Carter ◽  
Jeanie I. Brooks ◽  
William J. Brammar

1990 ◽  
Vol 183 (3) ◽  
pp. 1051 ◽  
Author(s):  
R.P. Rosenkranz ◽  
N.A. Sharif ◽  
S.F. Corkins ◽  
I. Lakatos ◽  
K.D. Lake ◽  
...  

1953 ◽  
Vol 98 (1) ◽  
pp. 71-80 ◽  
Author(s):  
George R. Meneely ◽  
Robert G. Tucker ◽  
William J. Darby ◽  
Stewart H. Auerbach

Sustained arterial hypertension developed in male, albino rats chronically fed diets rich in sodium chloride with demineralized drinking water available ad libitum. After 12 months of the experimental regimen a positive, linear correlation (r = 0.91) was found between the systolic blood pressure and the concentration of sodium chloride in the diet. A syndrome of edema and renal failure was observed in 18 per cent of the group fed at the level of 7.0 to 9.8 per cent of sodium chloride. Significant histologic changes occurred in the kidneys and certain other organs in rats consuming rations containing these levels of NaCl. The relative volume of the radiosodium space was increased in the rat by high dietary sodium chloride.


1992 ◽  
Vol 3 (2) ◽  
pp. 188-195
Author(s):  
G F DiBona ◽  
S Y Jones

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.


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