Cholecalciferol treatment changes urinary sodium–potassium ratio and plasma aldosterone of spontaneously hypertensive rats

2007 ◽  
Vol 376 (1-2) ◽  
pp. 253-254 ◽  
Author(s):  
Rosane de Souza Santos ◽  
Virgínia Alice Vieira da Costa ◽  
Lucia Marques Vianna
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Treatment Changes

Vascular Sodium—Potassium Pump Activity in Various Models of Experimental Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 179s-181s ◽  
Author(s):  
M. B. Pamnani ◽  
D. L. Clough ◽  
S. J. Huot ◽  
F. J. Haddy
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cell Membrane Permeability ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Primary Defect ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Sodium Potassium Pump

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension. 2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension. 3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.

scholarly journals Effects of dopamine on urinary sodium excretion in spontaneously hypertensive rats

1989 ◽  
Vol 30 (4) ◽  
pp. 593-593
Author(s):  
Yoko Jo ◽  
Takuzo Hano ◽  
Hideki Nishio ◽  
Kenji Ueshima ◽  
Masahiko Shiotani ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Body fluid volumes in prehypertensive spontaneously hypertensive rats

1983 ◽  
Vol 244 (5) ◽  
pp. H652-H655 ◽  
Author(s):  
M. M. Mullins
Keyword(s):  
Volume Expansion ◽  
Body Fluid ◽  
Spontaneously Hypertensive Rats ◽  
Interstitial Fluid ◽  
Extracellular Fluid ◽  
Plasma Aldosterone ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Total Body

To ascertain the effect of aldosterone on body fluid volumes in neonatal, prehypertensive spontaneously hypertensive rats (SHR), we studied these animals at 12 days using age-matched Wistar-Kyoto (WKY) as normotensive controls. Some pups of each strain were treated with spironolactone (1.5 micrograms/g body wt) on days 10-12. Total body water (TBW, by dessication) and extracellular fluid (ECF, Na2 35SO4 space) volumes were significantly larger in SHR than in WKY, whereas plasma volumes (125I-serum albumin space) were not different. Thus the enlarged ECF was due to preferential expansion of the interstitial fluid (ISF) space. Treatment of SHR with spironolactone reduced TBW and ISF to values not different from untreated WKY and also reduced plasma volume to some extent. These results indicate 1) significant ISF volume expansion occurs in SHR prior to elevation of blood pressure, and 2) the previously observed elevation in plasma aldosterone in SHR at this age probably mediates the volume expansion.

Renal Function and Sympathetic Activity during Mental Stress in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 327s-330s ◽  
Author(s):  
S. Lundin ◽  
P. Thorén
Keyword(s):  
Sodium Excretion ◽  
Sympathetic Activity ◽  
Mental Stress ◽  
Spontaneously Hypertensive Rats ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Renal Sympathetic

1. The role of the renal sympathetic nerves in the urinary sodium excretion response to ‘mental stress’ in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto normotensive (WKY) rats was examined. Urinary sodium excretion was measured during ‘rest’ and during a 20 min period of ‘mental stress’ in intact rats and in renal denervated rats. Under similar conditions renal sympathetic activity was also measured in a separate group of rats. 2. Urinary sodium excretion fell more during the stress period in SHR (-64 ± 5%) than in WKY rats (-34 ± 7%), despite a greater arterial pressure increase in SHR. This greater decrease in sodium excretion appeared to result from both a more pronounced reduction in GFR and a greater increase in tubular sodium reabsorbtion. 3. Renal sympathetic nerve activity, which was higher at rest in SHR than in WKY rats, increased much more in SHR than in WKY rats during stress. This may explain the greater reduction in sodium excretion in SHR during stress, because renal denervation almost abolished this latter response. 4. The neurogenically elicited renal response might contribute in an important way to the early development of SHR hypertension. Renal denervation, as well as attenuating sodium retention, also delays the pressure rise in the young SHR. 5. The initial tachycardia after mental stress gradually subsided towards the end of the stress period in SHR, whereas renal sympathetic activity remained elevated. This indicates that the increase in heart rate, if anything, may underestimate the true extent of sympathetic activation in for example the renal and splanchnic regions during arousal.

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