Differential effect of salt loading on sodium and lithium excretion in Dahl salt-resistant and -sensitive rats.
Fractional excretion of lithium, as a marker for proximal sodium reabsorption, was determined in normotensive Dahl S rats (susceptible to NaCl hypertension) and Dahl R rats (resistant to NaCl hypertension) before and following an acute sodium load. Baseline mean arterial pressures, inulin clearances, sodium excretion rates, and fractional lithium clearances were not different between the R and S rats. Following the salt loading and despite similar mean arterial pressures and degree of volume expansion, the glomerular filtration rate, urinary flow rates, and absolute sodium excretion rates were greater in R than S rats. The fractional excretion of lithium was also greater in R than S rats. These data demonstrate that, at equal mean arterial pressures, Dahl S rats have a reduced capacity for sodium excretion, and that this defect is present prior to the development of hypertension. Furthermore, the observation that these animals also have a lower fractional lithium excretion during volume expansion suggests that salt loading reduces proximal tubule reabsorption to a lesser extent in Dahl S than R rats. These data suggest that the subnormal sodium and water excretion observed after sodium loading in S rats may be partially due to an abnormality in proximal tubule sodium handling.
D000818:Animals; D001794:Blood Pressure; D005919:Glomerular Filtration Rate; D008094:Lithium / Q000652:urine*; D008297:Male; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D051381:Rats; D011922:Rats, Mutant Strains; D012964:Sodium / Q000494:pharmacology / Q000652:urine*
D008094:Lithium; D012964:Sodium; D011188:Potassium