Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in Angiotensin II‐induced hypertension

摘要: Aim Tubuloglomerular feedback (TGF) is an important mechanism in control of signal nephron glomerular filtration rate. The oxidative stress the macula densa, primarily determined by interactions between nitric oxide (NO) and superoxide (O2−), essential maintaining TGF responsiveness. However, few studies examining amount NO O2− generated densa during normal hypertensive states. Methods In this study, we used isolated perfused juxtaglomerular apparatus to directly measure also studied both physiological slow pressor Angiotensin II (Ang II)-induced mice. Results We found that Ang at a dose 600 ng kg−1 min−1 for two weeks increased mean arterial pressure 26.1 ± 5.7 mmHg. response from 3.4 ± 0.2 μm 5.2 ± 0.2 μm mice. We first measured generation it was undetectable 21.4 ± 2.5 unit II-induced then 138.5 ± 9.3 mice infused with II. Conclusions Under conditions, mainly controlled densa; induced hypertension, densa.