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Acta Physiologica 2009; Volume 196, Supplement 671
Scandinavian Physiological Society’s Annual Meeting
8/14/2009-8/16/2009
Uppsala, Sweden
REDUCTION IN NEPHRON NUMBER AND CHRONIC HIGH-SALT INTAKE CAUSE HYPERTENSION ROLE OF OXIDATIVE STRESS AND NITRIC OXIDE DEFICIENCY
Abstract number: O24
CARLSTROM1 M, SALLSTROM1 J, BROWN1 RD, PERSSON1 AEG
1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden. [email protected]
Background:
During the last decade there has been a great debate regarding the role of nephron endowment and the salt intake for the blood pressure level in the adult age. We have demonstrated that reduction in the number of nephrons, at young age, followed by chronic high- salt intake causes salt-sensitive hypertension in adult animals.
Aim:
In the present study we investigated the effect of nitric oxide stimulation or antioxidative treatment on blood pressure and tubuloglomerular feedback (TGF) response in hypertensive animals with reduced nephron number and chronic salt treatment.
Methods:
Rats were uninephrectomized (UNX) or sham-operated at 3-weeks of age and then subjected to high-salt diet (HS) or normal salt diet (NS), together with normal, L-arginine or tempol supplemented drinking water for 68 weeks, followed by blood pressure (telemetry) and TGF measurements.
Results:
Chronic salt-treatment caused hypertension in sham-operated controls (110±4 mmHg) which was augmented in UNX animals (144±8 mmHg), compared with non-treated controls (98±2 mmHg). L-arginine or tempol supplementation reduced blood pressure in both hypertensive groups, but had no significant effects in the controls. UNX+HS treated animals demonstrated an augmented TGF-response (increased reactivity and sensitivity), compared with the controls. Both L- arginine and tempol normalized the TGF-response, but had no effect in the controls.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 196, Supplement 671 :O24