Previous studies have shown that chronic low-dose administration of 40 ng/min
angiotensin II by osmotic minipump to uninephrectomized rats mimics the temporal hypertensive response and the circulating
angiotensin II levels observed in two-kidney, one
clip Goldblatt rats. Furthermore, renal tissue
angiotensin II contents were higher than the circulating
angiotensin II levels, suggesting that circulating
angiotensin II induces endogenous intrarenal
angiotensin II production. The present study examined the molecular mechanisms by which intrarenal
angiotensin II production is modulated in
angiotensin II-induced and two-kidney
Goldblatt hypertension. Two weeks after clipping, intrarenal
renin mRNA levels were elevated threefold in the clipped kidney of Goldblatt rats but were markedly suppressed in the nonclipped kidneys of Goldblatt rats (28% of control values) and in the remaining kidney of uninephrectomized
angiotensin II-infused rats (7% of control values). In contrast, there were sustained levels of
angiotensinogen mRNA in the kidneys and livers of Goldblatt and
angiotensin II-infused rats, indicating differential regulation of the genes of the renin-angiotensin system. Renal
kallikrein gene expression was not altered in either of the hypertensive groups 14 days after the induction of
hypertension, suggesting the absence of an enhanced counteracting
kinin influence.