Nitric oxide synthase I immunoreactivity in the macula densa of the kidney is angiotensin II dependent.

The present study was undertaken to clarify the mechanism of the regulation of nitric oxide synthase (NOS)-I in the macula densa of the kidney. We determined the changes in NOS-I immunoreactivity of the macula densa relevant to the changes in systemic blood pressure (BP) and the renin-angiotensin system. Rats received four different types of treatment, and kidney sections were immunohistochemically stained for renin, NOS-I, and NOS-III. Plasma renin activity (PRA) and angiotensin II (Ang II) concentration were determined by radioimmunoassay. In the low-salt group, PRA, plasma Ang II, and the number of renin and NOS-I positively stained areas in the juxtaglomerular apparatus (JGA) were all increased, while BP and NOS-III in the glomerular capillaries did not change. In the desoxycorticosterone acetate (DOCA)-salt group, in contrast to the elevation of BP, PRA, plasma Ang II, and all immunohistochemical parameters were decreased. In the Ang II infusion group, BP, plasma Ang II, and the number of NOS-I positive glomeruli were increased, while PRA and renin staining were decreased. Administration of Ang II type 1 receptor (AT-1) antagonist TCV-116 significantly increased PRA, plasma Ang II, and the number of renin-positive glomeruli. However, BP, and NOS-I and NOS-III staining did not show any difference. These results clearly suggest that NOS-I in the macula densa changes in parallel with plasma Ang II, but not renin or systemic BP.