Objective

To determine the response of systemic arterial blood pressure (BP) and renal function in response to variations in dietary sodium chloride (NaCl) intake in normal cats and in cats with renal insufficiency induced by one of two models.

Materials & Methods

The study comprised of twenty one cats, a normal cats (group 1) and cats underwent renal infarction (group 2) and renal wrapping (group 3). All cats were fed a standard diet that provided 50 mg of NaCl/kg and NaCl was supplemented to provide a total of 100 and 200 mg NaCl/kg/day for 6 days during each period. The BP was recorded continuously with a radio telemetric system and renal function (glomerular filtration rate; GFR and effective renal plasma flow (ERPF) was studied on the sixth day of each period of NaCl supplementation.

Results

The BP was significantly higher while heart rate (HR) was not different in groups 2 and 3. The variability of HR and BP were not different among groups and were not modified by dietary Na intake. In group 1, increased GFR and FF occurred in response to NaCl supplementation. However in cats with renal insufficiency, both GFR and ERPF were unaltered. Both GFR and ERPF were lower and filtration fraction higher in groups 2 and 3. The mean values for plasma renin activity (PRA) and plasma aldosterone concentration were increased in groups 2 and 3. The PRA and plasma aldosterone concentration were suppressed progressively in groups 2 and 3 in response to NaCl supplementation while there was no apparent change in group 1. The fractional excretions of both sodium (FE_Na) and potassium (FE_K) were significantly reduced after NaCl supplementation.

Conclusions

Cats with renal insufficiency had higher BP without changing HR and variability suggesting the resetting occurred after chronic hypertension and it was not modified by dietary Na. Dietary NaCl supplementation caused an increase in GFR without altering ERPF in normal cats, which may be due to afferent arteriolar dilatation in response to suppression of the RAA system. However, in groups 2 and 3 with renal impairment, the RAA system was overstimulated at the lower NaCl intake and NaCl supplementation did not change renal hemodynamics. Increased FE_K after NaCl supplementation was attributable to a reduction in aldosterone levels. However, other factors play an important role in controlling FE_Na in cats. The results suggest that supplement of Na in the diet had no effects on renal hemodynamics while RAA system are still overactivated in chronic renal insufficiency cats.