Does angiotensin II exert positive feedback on the intrarenal renin-angiotensin system by an angiotensin converting enzyme-dependent mechanism?
Incremental changes in plasma ANG II induce de novo production of ANG II in the non-ischemic kidney to augment intrarenal ANG II content. ACE inhibition blocks this positive feedback loop, suggesting that ANG II activates the intrarenal RAS by an ACE-dependent mechanism. The impact of ACE inhibition on blood pressure suggests that this feedback loop may be an important mechanism for maintenance of hypertension in RVH.
repeated administration of BMDCs reduced inflammation, fibrogenesis, and elastogenesis, thus improving lung mechanics through the release of paracrine factors.