Recent studies of our group have demonstrated that the blockade of angiotensin II effects during nephrogenic period reduces nephron number (37%) (Hypertension, in press) and the renal ability to eliminate an acute sodium load (American J Physiology, in press). It also induces the development of an age-dependent sodium sensitive hypertension. However, it remains unknown the mechanism responsible of this increment in arterial pressure. The aim of this study was to examine the role of angiotensin II in the hypertension elicited by the reduction of nephron number during renal development.

Sprague Dawley rats were treated with an angiotensin II AT1 receptor antagonist (ARA) (7 mg/Kg/day) or vehicle during the first 14 postnatal days. At 9-11 months of age, systolic arterial pressure was measured before and during the 3 days administration of an ARA (7 mg/Kg/day) to rats with normal (n=10) or low nephron number (n=10). ARA administration during 3 consecutive days induced a significant decrease of arterial pressure in control rats (114 ± 2 to 107 ± 2, p<0.05) and in rats with a reduced nephron number (143 ± 2 to 115 ± 3, p<0.05). Arterial pressure was significantly different in both groups before (P<0.05) but not after the prolonged blockade of AT1 receptors in the 9-11 months old rats.

The results of this study present new evidences demonstrating that the reduction of nephron number during nephrogenic period leads to an elevation in arterial pressure that is maintained by an activation of the renin-angiotensin system.