Abstract

Angiotensin II AT1 receptor (AT1R) and dopamine D1 receptor (D1R) are key kidney receptors involved in sodium metabolism and blood pressure regulation. Recently, we reported that aging in Fischer 344 X Brown Norway (FBN) rats is associated with higher renal AT1R and diminished D1R functions, while in Fischer 344 (F344) rats it is associated with only diminished D1R function. We tested the hypothesis that FBN and not F344 rats are salt sensitive during aging. Old (21-24 month) FBN and F344 rat strains were fed with high salt (HS, 8% NaCl) for 4 weeks and different parameters were measured. Both day (in mmHg; Control vs HS: 119+2 vs. 125+2) and night (in mmHg; Control vs HS: 116+2 vs. 123+2) blood pressures (BP) increased with HS in FBNs. BP did not change with HS in F344 rats (in mmHg; Control vs HS: 110+7 vs 111+9). Despite a similar food intake, there were marked decrease in body weight gain (in gm; Control vs HS: 38+7 vs 18+5) as well as fasting levels of blood glucose (in mg/dl; Control vs HS: 127+6 vs 105 + 4) and triglyceride (in mg/dl; Control vs HS: 157+14 vs 90+7) in HS fed compared to control FBNs. Plasma insulin and blood HDL cholesterol levels remained unchanged between HS fed and control FBNs. These results, together with our previous report, suggest that (1) both higher renal AT1R and diminished D1R function contributes to salt-sensitive hypertension in aging. (2) FBN and F344 rats may serve as useful aging models to study molecular targets that leads to and protect from the development of salt-sensitive hypertension, respectively, and (3) HS via changes in metabolic process may produce some beneficial effects.

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