Dietary Salt Aggravates Cyclosporin A-Induced Hypertension and Nephrotoxicity in Spontaneously Hypertensive Rats: Protection by Oral Magnesium Supplementation

2015 ◽  
pp. 121-124 ◽  
Author(s):  
Eero M. A Mervaala ◽  
Terttu-Liisa Ter�v�inen ◽  
Anna Kaisa Pere ◽  
Leena Lindgren ◽  
Juha Laakso ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Spontaneously Hypertensive Rats ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Magnesium Supplementation ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension ◽  
Oral Magnesium

Effects of Dietary Sodium and Magnesium on Cyclosporin A–Induced Hypertension and Nephrotoxicity in Spontaneously Hypertensive Rats

Hypertension ◽  
1997 ◽  
Vol 29 (3) ◽  
pp. 822-827 ◽  
Author(s):  
Eero M.A. Mervaala ◽  
Anna-Kaisa Pere ◽  
Leena Lindgren ◽  
Juha Laakso ◽  
Terttu-Liisa Teräväinen ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Spontaneously Hypertensive Rats ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension

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.

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