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Am J Physiol Regul Integr Comp Physiol 279: R1099-R1104, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 3, R1099-R1104, September 2000

Sodium homeostasis in transplanted rats with a spontaneously hypertensive rat kidney

Bernd A. J. Frey1, Olaf Grisk1, Norman Bandelow1, Siegfried Wussow1, Peter Bie2, and Rainer Rettig1

1 Department of Physiology, Ernst Moritz Arndt University Greifswald, D-17495 Karlsburg, Germany; and 2 Department of Physiology, Odense University, DK-5000 Odense C, Denmark

Recipients of a kidney from spontaneously hypertensive rats (SHR) but not from normotensive Wistar-Kyoto rats (WKY) develop posttransplantation hypertension. To investigate whether renal sodium retention precedes the development of posttransplantation hypertension in recipients of an SHR kidney on a standard sodium diet (0.6% NaCl), we transplanted SHR and WKY kidneys to SHR × WKY F1 hybrids, measured daily sodium balances during the first 12 days after removal of both native kidneys, and recorded mean arterial pressure (MAP) after 8 wk. Recipients of an SHR kidney (n = 12) retained more sodium than recipients of a WKY kidney (n = 12) (7.3 ± 10 vs. 4.0 ± 0.7 mmol, P < 0.05). MAP was 144 ± 6 mmHg in recipients of an SHR kidney and 106 ± 5 mmHg in recipients of a WKY kidney (P < 0.01). Modest sodium restriction (0.2% NaCl) in a further group of recipients of an SHR kidney (n = 10) did not prevent posttransplantation hypertension (MAP, 142 ± 4 mmHg). Urinary endothelin and urodilatin excretion rates were similar in recipients of an SHR and a WKY kidney. Transient excess sodium retention after renal transplantation may contribute to posttransplantation hypertension in recipients of an SHR kidney.

hypertension; transplantation


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