Influence of Salt Loading on the Cardiac and Renal Preproendothelin-1 mRNA Expression in Stroke-Prone Spontaneously Hypertensive Rats

1995 ◽  
Vol 209 (1) ◽  
pp. 161-166 ◽  
Author(s):  
O. Feron ◽  
S. Salomone ◽  
T. Godfraind
Keyword(s):  
Mrna Expression ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

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.

A Deficit in preprodynorphin mRNA expression in hippocampus of spontaneously hypertensive rats

1994 ◽  
Vol 23 (4) ◽  
pp. 345-348 ◽  
Author(s):  
John Q. Wang ◽  
Sijia Li ◽  
Alphonse J. Ingenito ◽  
Jacqueline F. McGinty
Keyword(s):  
Mrna Expression ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Comparison of BASP1 and MARCKS protein exchange traits in the kidneys of rats with spontaneous

2020 ◽  
pp. 19-26
Author(s):  
Анна Сергеевна Альдекеева
Keyword(s):  
Mrna Expression ◽  
Spontaneously Hypertensive Rats ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Tissue Samples ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
Interlinear Differences ◽  
Mrna Expression Levels ◽  
Marcks Protein

Исследовали возможные различия в обмене белков BASP1 и MARCKS в почках крыс со спонтанной гипертензией (линияSHR), путем сравнения уровней экспрессии мРНК этих белков в различных структурах почек. Работа выполнена на самцах крыс линии SHR (n=8) и крыс линии WKY (n=8), в возрасте 90 дней. Исследование проводили на образцах ткани из коркового и мозгового слоев почек. Уровни экспрессии мРНК BASP1 и MARCKS определяли методом ПЦР в реальном времени. Обнаружены достоверные различия (p<0.001) уровней экспрессии мРНК BASP1 и MARCKS между корковыми и мозговыми слоями почек у крыс линий SHR и WKY. При этом межлинейные различия в уровнях экспрессии мРНК обоих белков практически отсутствовали (p=0.050). Показано, что неравномерное распределение уровней экспрессии мРНКбелков BASP1 и MARCKS в мозговом и корковом слоях почек не зависит от уровня артериального давления и наличия спонтанной гипертензии This study aims to detect differences in BASP1 and MARCKS protein metabolisms in kidneys of spontaneously hypertensive rats by comparing their mRNA expression in different kidney structures. The work was performed on 90 days old male SHR (n = 8) and WKY (n = 8) rats. The study was carried out on tissue samples from cortical and medullar kidney layers. BASP1 and MARCKS mRNA expression levels were determined by real-time PCR. Significant differences (p <0.001) in the expression levels of BASP1 and MARCKS mRNA between cortical and medullar kidney layers in both SHR and WKY strain rats were found. Moreover, interlinear differences in the levels of both proteins’ mRNA expression were practically absent (p = 0.050). It was shown that uneven distribution of mRNA expression levels of BASP1 and MARCKS mRNA in kidneys medullar and cortical layers does not depend on the level of blood pressure and the presence of spontaneous hypertension.

scholarly journals Salt loading decreases urinary excretion and increases intracellular accumulation of uromodulin in stroke-prone spontaneously hypertensive rats.

2021 ◽  
Author(s):  
Sheon Mary ◽  
Philipp Boder ◽  
Giacomo Rossitto ◽  
Lesley Graham ◽  
Kayley Scott ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Ex Vivo ◽  
Chronic Hypertension ◽  
Thick Ascending Limb ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

Uromodulin (UMOD) is the most abundant renal protein secreted into urine by the thick ascending limb (TAL) epithelial cells of the loop of Henle. Genetic studies have demonstrated an association between UMOD risk variants and hypertension. We aimed to dissect the role of dietary salt in renal UMOD excretion in normotension and chronic hypertension. Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) (n=8/sex/strain) were maintained on 1% NaCl for three weeks. A subset of salt-loaded SHRSP was treated with nifedipine. Salt-loading in SHRSP increased blood pressure (ΔSBP 35 ± 5 mmHg, p&lt;0.0001) and kidney injury markers such as KIM-1 (fold change, FC 3.4; p=0.003), NGAL (FC, 2.0; p=0.012) and proteinuria. After salt-loading there was a reduction in urinary UMOD excretion in WKY and SHRSP by 26% and 55% respectively, compared to baseline. Nifedipine treatment reduced blood pressure in SHRSP, however, did not prevent salt-induced reduction in urinary UMOD excretion. In all experiments, changes in urinary UMOD excretion were dissociated from kidney UMOD protein and mRNA levels. Colocalization and ex-vivo studies showed that salt-loading increased intracellular UMOD retention in both WKY and SHRSP. Our study provides novel insights into the interplay between salt, UMOD, and blood pressure. The role of UMOD as a cardiovascular risk marker deserves mechanistic reappraisal and further investigations based on our findings.

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