Morphology of the adrenal cortex in normo- and hypertensive rats under conditions of salt loading

1994 ◽  
Vol 118 (6) ◽  
pp. 1340-1343
Author(s):  
B. N. Tsibel' ◽  
S. S. Golubev ◽  
A. Ya. Terner
Keyword(s):  
Adrenal Cortex ◽  
Hypertensive Rats ◽  
Salt Loading

Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats

2007 ◽  
Vol 292 (2) ◽  
pp. H814-H819 ◽  
Author(s):  
Luis C. Matavelli ◽  
Xiaoyan Zhou ◽  
Jasmina Varagic ◽  
Dinko Susic ◽  
Edward D. Frohlich
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Plasma Flow ◽  
Spontaneously Hypertensive Rats ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

We have previously shown that salt excess has adverse cardiac effects in spontaneously hypertensive rats (SHR), independent of its increased arterial pressure; however, the renal effects have not been reported. In the present study we evaluated the role of three levels of salt loading in SHR on renal function, systemic and renal hemodynamics, and glomerular dynamics. At 8 wk of age, rats were given a 4% ( n = 11), 6% ( n = 9), or 8% ( n = 11) salt-load diet for the ensuing 8 wk; control rats ( n = 11) received standard chow (0.6% NaCl). Rats had weekly 24-h proteinuria and albuminuria quantified. At the end of salt loading, all rats had systemic and renal hemodynamics measured; glomerular dynamics were specially studied by renal micropuncture in the control, 4% and 6% salt-loaded rats. Proteinuria and albuminuria progressively increased by the second week of salt loading in the 6% and 8% salt-loaded rats. Mean arterial pressure increased minimally, and glomerular filtration rate decreased in all salt-loaded rats. The 6% and 8% salt-loaded rats demonstrated decreased renal plasma flow and increased renal vascular resistance and serum creatinine concentration. Furthermore, 4% and 6% salt-loaded rats had diminished single-nephron plasma flow and increased afferent and efferent arteriolar resistances; glomerular hydrostatic pressure also increased in the 6% salt-loaded rats. In conclusion, dietary salt loading as low as 4% dramatically deteriorated renal function, renal hemodynamics, and glomerular dynamics in SHR independent of a minimal further increase in arterial pressure. These findings support the concept of a strong independent causal relationship between salt excess and cardiovascular and renal injury.

Renin-angiotensin system in stroke-prone spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. H409-H416 ◽  
Author(s):  
M. Shibota ◽  
A. Nagaoka ◽  
A. Shino ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.

scholarly journals The Influences of Salt Loading on Spontaneously Hypertensive Rats

1977 ◽  
Vol 18 (4) ◽  
pp. 575-576 ◽  
Author(s):  
Noboru SAITO ◽  
Sakae MUKAINO ◽  
Koichi OGINO
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

Further analysis of cell membrane changes in genetic hypertension in rats by diphenylhexatriene fluorescence polarization

1984 ◽  
Vol 66 (6) ◽  
pp. 717-723 ◽  
Author(s):  
I. Aracon-Birlouez ◽  
T. Montenay-Carestier ◽  
M. A. Devynck
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Erythrocyte Membranes ◽  
Shr Rats ◽  
Erythrocyte Ghosts ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Platelet Membranes ◽  
Wistar Kyoto ◽  
Membrane Changes

1. Fluorescence Dolarization of dbhenvlhexa-triene embedded in membranes was used as an index of ‘microviscosity’ in platelets and ervthro—cyte ghosts of spontaneously hypertensive rats of the Okamoto-Aoki strain (SHR), Wistar-Kyoto strain (WKY) and of the hypertension-prone and -resistant Sabra strains (SBH and SBN), and the original Sabra strain (SB). 2. Microviscosity was increased both in erythrocyte ghosts and platelet membranes of male but not female SHR rats compared with WKY rats and in hypertension-prone Sabra rats compared with the original Sabra rats. 3. Acute and chronic salt loading increased the microviscosity of platelet membranes in all strains of rats but had no effect on the erythrocyte membranes. 4. Microviscosities of vesicles made of lipids extracted from SHR and WKY erythrocyte ghosts were similar. This supports the hypothesis that membrane proteins play a major role in the differences in microviscosity observed in SHR rats.

Renal Urinary Kallikrein in Normotensive and Hypertensive Rats during Enhanced Excretion of Water and Electrolytes

1976 ◽  
Vol 51 (s3) ◽  
pp. 259s-261s ◽  
Author(s):  
H. R. Croxatto ◽  
R. Albertini ◽  
R. Arriagada ◽  
J. Roblero ◽  
M. Rojas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Kallikrein ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Water Loading ◽  
Equal Degree ◽  
Renal Kallikrein

1. Urinary kallikrein excreted by normal rats is significantly increased (P < 0·001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0·27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion (P < 0·01) but considerably increased sodium excretion (P < 0·001). 2. Renal kallikrein, measured by its kininogenase activity within 2 h of water loading, was significantly increased (P < 0·05); after water loading and frusemide it was 40% decreased (P < 0·001) and after salt loading it was reduced by approximately 50% (P < 0·02). Renin did not change renal kallikrein. 3. Severely hypertensive (one-kidney) rats (blood pressure >150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis; in moderately hypertensive rats (blood pressure <150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.

Vascular Lesions in Hypertensive Rats under Salt Loading: Kidney Renin and Lysosomal Enzymes

1976 ◽  
Vol 51 (s3) ◽  
pp. 49s-51s
Author(s):  
N. Saito ◽  
S. Mukaino ◽  
K. Ogino ◽  
C. Kawai
Keyword(s):  
Enzyme Activities ◽  
Cathepsin D ◽  
Normal Diet ◽  
High Salt ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. β-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13–14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.

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