ラット腎nitric oxide synthase(NOS)の発現動態とrenin-angiotensin系との関連における免疫組織学的研究

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It has become increasingly evident that ntiric oxide (NO) plays an improtant role in the regulation of renal hemodynamics and tubular function based on interactions with the renin-angiotensin system. NO synthase (NOS) produces NO and has recently been demonstrated to be present in the kidney. We determined the changes in intrarenal NOS immunoreactivity relevant to the changes in systemic blood pressure and the renin-angiotensin system. Rats received 4 different types of treatment, and kidney sections were immunohistochemically stained for renin, NOS-I, and NOS-III. Plasma renin activity (PRA) and the angiotensin II (AngII) 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 blood pressure (BP) and NOS-III in the glomerular capillaries were un-changed. In the desoxycorticosterone acetate (DOCA)-salt group, in contrast, BP was elevated, but 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 the Ang II type 1 receptor (AT1) antagonist TCV-116 significantly increased PRA, plasma AngII, and the number of renin-positive glomeruli. However, BP, and NOS-I and NOS-III staining did not differ. These results indicate that NOS-I in the macula densa changes in parallel with plasma Ang II but not renin or systemic BP.
東京女子医科大学の論文
1998-05-25

ラット腎nitric oxide synthase(NOS)の発現動態とrenin-angiotensin系との関連における免疫組織学的研究

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