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

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 292; no. 2; pp. H814 - H819
• Main Authors: Matavelli, Luis C, Zhou, Xiaoyan, Varagic, Jasmina, Susic, Dinko, Frohlich, Edward D
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.02.2007
• Subjects: Albuminuria - blood; Albuminuria - etiology; Albuminuria - pathology; Albuminuria - physiopathology; Animals; Blood pressure; Blood Pressure - drug effects; Body Weight - drug effects; Cardiovascular disease; Creatinine - blood; Dose-Response Relationship, Drug; Glomerular Filtration Rate - drug effects; Kidney - blood supply; Kidney - drug effects; Kidney - pathology; Kidney diseases; Kidney Function Tests; Male; Nephrosclerosis - etiology; Nephrosclerosis - physiopathology; Organ Size - drug effects; Proteinuria - blood; Proteinuria - etiology; Proteinuria - pathology; Proteinuria - physiopathology; Rats; Rats, Inbred SHR; Renal Circulation - drug effects; Rodents; Sodium; Sodium Chloride, Dietary - adverse effects; Time Factors; Vascular Resistance - drug effects; Water-Electrolyte Balance - drug effects
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00671.2006

Hypertension Research Laboratory, Division of Research, Ochsner Clinic Foundation, New Orleans, Louisiana Submitted 23 June 2006 ; accepted in final form 18 September 2006 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. sodium; renal effects; glomerular injury; albuminuria Address for reprint requests and other correspondence: E. D. Frohlich, Ochsner Clinic Foundation, 1516 Jefferson Hwy., New Orleans, LA 70121 (e-mail: efrohlich{at}ochsner.org )