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MINERVA UROLOGICA E NEFROLOGICA

A Journal on Nephrology and Urology


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Minerva Urologica e Nefrologica 2010 September;62(3):225-9

language: English

Sodium sensitivity and its role in the maintenance of high blood pressure in two-kidney, one-clip renovascular hypertension after remova of the clipped kidney in rats

Kalaitzis C. 1, Pasadakis P. 2, Bantis A. 1, Giannakopoulos S. 1, Touloupidis S. 1

1 Department of Urology, University of Thrace, Alexandroupolis, Greece;
2 Department of Nephrology, University of Thrace, Alexandroupolis, Greece


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AIM: The aim of the present study was to define the role of sodium balance and sodium sensitivity in the maintenance of two-kidney, one-clip renovascular hypertension in rats.
METHODS: Six months after induction of hypertension, systolic blood pressure, sodium balance, water intake and urine excretion were measured under normal conditions, after nephrectomy of the clipped kidney, and under conditions of sodium load.
RESULTS: No difference between control rats and rats with or without post-Goldblatt hypertension emerged during the development of renovascular hypertension and after nephrectomy of the clipped kidney. Under conditions of high sodium intake, the contalateral kidney of the post-Goldblatt hypertensive rats was unable to excrete surplus sodium. Sodium retention was not correlated with water retention. In contrast to the controls, systolic blood pressure increased in the animals with post-Goldblatt hypertension and those with post-Goldblatt normotension during the sodium load period. No correlation was found between blood pressure increase and sodium retention. The animals were considered sodium sensitive in relation to blood pressure.
CONCLUSION: In the chronic phase of two kidney-one clip renovascular hypertension, the post-Goldblatt hypertensive and the post-Goldblatt normotensive animals showed sodium sensitivity of blood pressure. The contralateral kidney of the post-Goldblatt hypertensive animals was unable to excrete surplus sodium under conditions of high sodium intake. But this inability and the sodium sensitivity of blood pressure cannot be thought responsible for the maintenance of renovascular hypertension in this model.

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