Jørgen Frøkiær

Essential hypertension is associated with an exaggerated natriuresis in response to intravenous infusion of isotonic saline. We examined proximal tubular fluid output and segmental tubular handling of sodium in conscious spontaneously hypertensive rats (SHR), their normotensive counterparts Wistar-Kyoto rats (WKY), and ordinary Wistar rats using servo-controlled sodium and fluid balance and Li clearance technique. Sodium (Na) excretion rose to 2.72 ± 0.75 (by a factor of 8) and 1.73 ± 0.68 μmol/min (by a factor of 6.3) (p < 0.05) in SHR and WKY, respectively, thus confirming the presence of exaggerated natriuresis in SHR. FE(Li) rose to 34 ± 4 and 29 ± 2 (p < 0.05) and C(Na)/C(Li) rose to 3.0 ± 0.8 and 2.0 ± 0.6 (p < 0.05) in SHR and WKY, respectively, demonstrating that Na reabsorption in both the proximal and the distal nephron was involved. Additional experiments showed that giving the rats saline instead of water to drink for four days prior to the clearance measurement led to a remarkable increase in the natriuretic response to volume expansion. There was a close correlation between the peak increase in FE(Na) and the logarithmic values of the baseline FE(Na) values. In conclusion, the study confirms the presence of an exaggerated natriuresis in response to volume expansion in conscious SHR rats compared to WKY rats, and that the renal response to acute volume expansion is related to the baseline sodium excretion.