Key result
Two-kidney, one-clip (2K1C) renovascular hypertension in mice led to increased reactive oxygen species, DNA fragmentation (54%), and apoptosis (21%) in bone marrow cells at 2 weeks.
Renovascular hypertension may injure bone marrow cells; leaves open human relevance and requires translational studies.
Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.
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Campagnaro et al. (2013) studied Renovascular Hypertension. Two-kidney, one-clip (2K1C) renovascular hypertension vs. Sham operation was evaluated on Oxidative stress, DNA fragmentation, and apoptosis of bone marrow cells. Two-kidney, one-clip (2K1C) renovascular hypertension in mice led to increased reactive oxygen species, DNA fragmentation (54%), and apoptosis (21%) in bone marrow cells at 2 weeks.
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