The Hypertensive Role of the Kidney in Spontaneously Hypertensive Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 135s-139s ◽  
Author(s):  
G. Bianchi ◽  
U. Fox ◽  
G. F. Di Francesco ◽  
U. Bardi ◽  
Maria Radice
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
High Salt ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
Wistar Strain

1. Spontaneously hypertensive and normotensive rats were selectively bred from a single Wistar strain. 2. Cross-transplantation of kidneys from hypertensive to normotensive rats and vice versa was performed, the sole remaining kidney of the recipient later being excised. Kidneys were also transplanted from normotensive donors into normotensive recipients and from hypertensive to hypertensive. 3. Normotensive rats receiving a kidney from either a hypertensive or normotensive donor showed unchanged blood pressure on normal salt diet. High-salt diet produced a greater rise in recipients of hypertensive than in recipients of normotensive kidneys. 4. Normotensive kidneys reduced the blood pressure of hypertensive recipients, but transplanted hypertensive kidneys had no such effect.

scholarly journals Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 439-443 ◽  
Author(s):  
Carlos Labat ◽  
Patrick Lacolley ◽  
Malika Lajemi ◽  
Marc de Gasparo ◽  
Michel E. Safar ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Carotid Artery ◽  
Spontaneously Hypertensive Rats ◽  
High Salt ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Spontaneously Hypertensive

Genetic linkage of albuminuria and renal injury in Dahl salt-sensitive rats on a high-salt diet: comparison with spontaneously hypertensive rats

2004 ◽  
Vol 18 (2) ◽  
pp. 218-225 ◽  
Author(s):  
Anja-Kristin Siegel ◽  
Peter Kossmehl ◽  
Michael Planert ◽  
Angela Schulz ◽  
Markus Wehland ◽  
...  
Keyword(s):  
Renal Injury ◽  
Spontaneously Hypertensive Rats ◽  
High Salt ◽  
Hypertensive Rats ◽  
Tubulointerstitial Injury ◽  
High Salt Diet ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
Damage Indices ◽  
Salt Sensitive Hypertension

Our aim was to study the effects of high-salt diet on the genetics of albuminuria and renal injury in the Dahl salt-sensitive (SS) rat. We compared SS with salt-resistant spontaneously hypertensive rats (SHR) and with genetically related salt-sensitive stroke-prone SHR (SHRSP). Moreover, we performed genome-wide linkage analysis to identify quantitative trait loci (QTL) contributing to salt-induced renal injury in an F2 population derived from SS and SHR ( n = 230). In response to high-salt diet SS and SHRSP developed a striking increase in systolic blood pressure, urinary albumin excretion (UAE), and renal damage indices compared with SHR. Both SHRSP and SS developed severe glomerulosclerosis, whereas microangiopathy, tubulointerstitial fibrosis, and inflammation were more pronounced in SHRSP. We detected two QTL with significant linkage to UAE on rat chromosomes (RNO) 6 and 19. Comparison with the recently identified salt-independent UAE QTL in young animals revealed that the UAE QTL on RNO6 is unique to high-salt conditions, whereas RNO19 plays a significant role during both low- and high-salt conditions. Some F2 animals demonstrated severe microangiopathy and tubulointerstitial injury, which exceeded the degree observed in the parental SS strain. Three loci demonstrated suggestive linkage to these phenotypes on RNO3, RNO5, and RNO20, whereas no linkage to glomerular damage was found. Further analyses at these loci indicated that the severity of renal injury was attributable to the SHR allele. Our data suggest that the SHR genetic background confers greater susceptibility for the development of microangiopathy and tubulointerstitial injury in salt-sensitive hypertension than the SS background.

scholarly journals Posterior reversible encephalopathy syndrome in stroke-prone spontaneously hypertensive rats on high-salt diet

2018 ◽  
Vol 39 (7) ◽  
pp. 1232-1246 ◽  
Author(s):  
Fanny Herisson ◽  
Iris Zhou ◽  
Jerome Mawet ◽  
E Du ◽  
Arnavaz H Barfejani ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Small Vessel Disease ◽  
High Salt ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
Posterior Reversible Encephalopathy ◽  
Vessel Disease ◽  
Reversible Encephalopathy

Stroke-prone spontaneously hypertensive rats (SHRSP) on high-salt diet are characterized by extremely high arterial pressures, and have been endorsed as a model for hypertensive small vessel disease and vascular cognitive impairment. However, rapidly developing malignant hypertension is a well-known cause of posterior reversible encephalopathy syndrome (PRES) in humans, associated with acute neurological deficits, seizures, vasogenic cerebral edema and microhemorrhages. In this study, we aimed to examine the overlap between human PRES and SHRSP on high-salt diet. In SHRSP, arterial blood pressure progressively increased after the onset of high-salt diet and seizure-like signs emerged within three to five weeks. MRI revealed progressive T2-hyperintense lesions suggestive of vasogenic edema predominantly in the cortical watershed and white matter regions. Histopathology confirmed severe blood–brain barrier disruption, white matter vacuolization and microbleeds that were more severe posteriorly. Hematological data suggested a thrombotic microangiopathy as a potential underlying mechanism. Unilateral common carotid artery occlusion protected the ipsilateral hemisphere from neuropathological abnormalities. Notably, all MRI and histopathological abnormalities were acutely reversible upon switching to regular diet and starting antihypertensive treatment. Altogether our data suggest that SHRSP on high-salt diet recapitulates the neurological, histopathological and imaging features of human PRES rather than chronic progressive small vessel disease.

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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