The renin-angiotensin system (RAS) plays a crucial role in the regulation of blood pressure, however, excessive stimulation of renin-producing cells in the kidney due to the possible effects of RAS inhibitors could lead to vascular diseases with adverse consequences.
Hypertension affects more than 1.3 billion people worldwide. This condition forces the heart to work excessively, which can cause other serious problems, such as stroke, myocardial infarction, kidney damage, and vision loss, among others.
The renin-angiotensin system (RAS) plays a crucial role in regulating blood pressure. Renin is a hormone enzyme produced by kidney cells that is stimulated when blood pressure drops. RAS inhibitors are widely and effectively used to control hypertension. They are quite safe when used under a doctor’s supervision, but signs of possible kidney damage, such as reduced frequency of urination, swelling of the legs or feet, or seizures, should be reported as soon as possible. In any case, the possible effects of chronic RAS inhibition on the kidney are well known, even if the reason that causes these harmful alterations is not yet entirely clear.
Now, a team of researchers from the University of Virginia School of Medicine (USA) has discovered that long-term treatment of hypertension with renin-angiotensin system (RAS) inhibitors could destroy the kidneys’ ability to filter and purify blood. blood. “We need to accurately understand the effects of long-term use of RAS inhibitors on the kidneys,” says researcher R. Ariel Gomez of the UVA Research Center.
According to what these authors published in the journal Circulation Research, excessive stimulation of renin-producing cells in the kidney causes the cells to return to an invasive embryonic state. In this state, the cells lining the tiny arteries of the kidney begin to overgrow and begin to secrete renin and substances that trigger other changes: new nerves grow like weeds, immature smooth muscle cells accumulate, scars form around the tiny arteries. called arterioles and inflammatory cells infiltrate. The end result is a “silent but serious” vascular disease, the researchers point out.
““Our 3D images clearly revealed that long-term inhibition of the RAS leads to hyperinnervation of the renal arteries,along with arteriolar hypertrophy and infiltration of inflammatory immune cells.”said researcher Manako Yamaguchi. “This neuroimmune-endocrine cooperation synergistically promotes increased renin production to maintain blood pressure homeostasis, but, on the other hand, severe arteriolar hypertrophy reduces the blood filtration function of the kidney..
The findings of these researchers could open new avenues for the prevention of adverse effects in the treatment of hypertension. “Our next goal is to elucidate the complete picture of interactions between renin cells,smooth muscle cells,nerves,and inflammatory cells under RAS inhibition.“said another researcher, María Luisa S. Sequeira-López. LDB/MTT (SyM)