In situ localization of renin and its mRNA in neonatal ureteral obstruction

Angiotensin II is an important mediator of renal vasoconstriction resulting from chronic unilateral ureteral obstruction (UUO). Distribution of renin mRNA and immunoreactive renin (IR) was examined in kidneys of 1-mo-old Sprague-Dawley rats subjected to either sham operation (n = 21), left complete UUO (n = 21), or right uninephrectomy (UNX, n = 16) at 2 days of age. There were no differences among the three groups in mean arterial pressure or plasma renin activity. Unlike sham kidneys, in which IR was detected in less than 55% of juxtaglomerular apparatuses (JGA) and was confined to a juxtaglomerular location, IR in both kidneys of animals with UUO appeared in greater than 75% of JGA and extended along most of the length of the afferent arteriole (P less than 0.01). In contrast, IR in kidneys of UNX rats was localized to the JGA as in sham-operated animals. Compared with sham-operated kidneys, renal renin content was increased in the obstructed kidneys (P less than 0.01) but decreased in the intact opposite kidneys of UUO rats and in the remaining kidneys of UNX rats (P less than 0.05). Renin mRNA, detected by in situ hybridization histochemistry, was localized to the JGA in kidneys of all groups. However, the fraction of JGA containing detectable renin mRNA was higher in obstructed kidneys than in intact opposite, UNX, or sham kidneys (P less than 0.05). In conclusion, UUO alters intrarenal renin independent of the systemic renin-angiotensin system. The greater distribution of IR, increased renin content, and renin gene expression of kidneys with ipsilateral UUO are consistent with a role for renin-angiotensin in mediating the vasoconstriction resulting from UUO.