Proceedings of The Physiological Society

University College Dublin (2009) Proc Physiol Soc 15, C32

Oral Communications

High sodium diet modifies renal vascular responses in Wistar rats

K. Olszynski1, M. Kuczeriszka1, B. Badzynska1, A. Walkowska1, E. Kompanowska-Jezierska1

1. Laboratory of Renal and Body Fluid Physiology, M Mossakowski Medical Centre, Warsaw, Poland.

High salt intake is a known risk factor in the development of hypertension and related kidney damage. Changes in renal blood vessel function and morphology may also be directly related to consequences of high salt intake other than hypertension, such as hypernatremia, altered reactivity to vasoactive agents, oxidative stress or inflammatory process. The aim of our study was to examine the impact of high salt diet on the reactivity of intrarenal vasculature estimated on basis of changes in intrarenal regional perfusion. The experiments were approved by the First Warsaw Ethical Committee. In male rats maintained on standard (STD, 0.25% Na w/w) or high sodium diet (HS 4% Na w/w) for 3 weeks, systolic blood pressure (SBP, tail cuff method), plasma sodium (PNa) and osmolality (Posm) were measured repeatedly (HS, n=15; STD, n=6). After 3 weeks rats were anaesthetized (sodium thiopental, 100 mg/kg, i.p.) and 10-min infusions of acetylcholine (Ach, 5 and 10 µg/kg/h) and noradrenaline (NA, 10 and 30 µg/kg/h) were given via renal artery, in random order (HS, n=6; STD, n=4). Total renal blood flow (RBF, Transonic probe) and cortical (CBF), outer- and inner medullary (OMBF, IMBF) blood flows (laser-Doppler technique) were measured. The mean values of all the parameters were compared using ANOVA and Student t test for dependent or independent samples, as appropriate. From 16th day of HS diet, SBP became higher than in STD rats (163±3 vs. 140±13 mmHg, P<0.05). PNa did not change significantly but Posm increased during high sodium intake. RBF, CBF and IMBF (but not OMBF) tended to increase in HS rats, which resulted in a reduction of the OMBF/IMBF ratio. In HS rats the increase in CBF in response to Ach (10 µg/kg/h) was significantly smaller than in STD rats (33±10 vs. 57±15 Perfusion Units, P<0.05). For outer and inner medulla, the vasodilator response to Ach (5 µg/kg/h) was visibly impaired compared to that in STD rats (15±10 vs. 40±18 PU for OMBF and 6±7 vs. 32±20 PU for IMBF, respectively). In HS rats the dose dependence of the response to NA was visibly diminished for RBF and completely abolished for CBF. The decrease in CBF in response to the higher dose of NA was significantly less in HS than in STD rats (6±1 vs. 25±3 %, respectively, P<0.001). Our measurements of intrarenal regional perfusion confirm that changes in Na intake alter renal vascular reactivity to vasoactive agents. On high Na diet the ability of the renal cortex and medulla to vasodilate was distinctly impaired. The relative resistance to vasodilatation in the renal medulla, the region crucial for the control of arterial blood pressure, could contribute to the rise in the pressure observed in HS rats. On the other hand, high Na intake appeared also to limit the cortical vasoconstrictor response to NA, which could help maintain glomerular filtration and renal excretion.

Where applicable, experiments conform with Society ethical requirements