scholarly journals Cardiovascular and Renal Effects of the Combination of Felodipine and Metoprolol During a High-Salt and a Moderate-Salt Diet in Spontaneously Hypertensive Rats

1997 ◽  
Vol 61 (5) ◽  
pp. 421-431 ◽  
Author(s):  
Eero M.A. Mervaala ◽  
Terttu-Liisa Teräväinen ◽  
Lena Malmberg ◽  
Juha Laakso ◽  
Ilkka Pörsti ◽  
...  
Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 439-443 ◽  
Author(s):  
Carlos Labat ◽  
Patrick Lacolley ◽  
Malika Lajemi ◽  
Marc de Gasparo ◽  
Michel E. Safar ◽  
...  

2004 ◽  
Vol 18 (2) ◽  
pp. 218-225 ◽  
Author(s):  
Anja-Kristin Siegel ◽  
Peter Kossmehl ◽  
Michael Planert ◽  
Angela Schulz ◽  
Markus Wehland ◽  
...  

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.


1973 ◽  
Vol 45 (s1) ◽  
pp. 135s-139s ◽  
Author(s):  
G. Bianchi ◽  
U. Fox ◽  
G. F. Di Francesco ◽  
U. Bardi ◽  
Maria Radice

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.


2018 ◽  
Vol 39 (7) ◽  
pp. 1232-1246 ◽  
Author(s):  
Fanny Herisson ◽  
Iris Zhou ◽  
Jerome Mawet ◽  
E Du ◽  
Arnavaz H Barfejani ◽  
...  

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.


1997 ◽  
Vol 356 (1) ◽  
pp. 107-114 ◽  
Author(s):  
E. M. A. Mervaala ◽  
Lena Malmberg ◽  
Terttu-Liisa Teräväinen ◽  
Tuula Lähteenmäki ◽  
Kirsi Karjala ◽  
...  

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