Losartan protects mesenteric arteries from ROS-associated decrease in myogenic constriction following 5/6 nephrectomy.

Background: Chronic renal failure (CRF) is associated with hypertension, proteinuria, loss of myogenic constriction (MC) of mesenteric arteries and increased production of reactive oxygen species (ROS) under experimental conditions. Previous results showed that ACE (angiotensin-converting enzyme activity) inhibitor therapy is effective in slowing down the progression of disease. Therefore, we wanted to study whether the inverse AT(1) (angiotensin II type 1) receptor agonist, losartan (LOS) was effective in preventing loss of MC in a rat model of CRF and whether acute ROS scavengers could improve MC.

Possible new druggable targets for the treatment of nephrosis. Perhaps we should find them in caveolea?

Nephrosis refers to a condition resulting from proteinuric kidney disease, leading to irreversible renal parenchymal damage and end-stage renal disease when left untreated. Furthermore, nephrosis appears to be a communicable disease carrying risks and complications to other organs such as the heart. Key pathophysiolgical processes involved in initiating and progressing renal damage in nephrosis and its complications may include altered glomerular hemodynamics after initial renal damage and loss of nephrons, nephrotoxicity of increased renal protein traffic enforcing intrinsic 'common pathway' mechanisms of renal scarring, and generalized endothelial dysfunction proceeding CV disease.

The role of angiotensin(1-7) in renal vasculature of the rat.

Objective: Angiotensin(1-7) is an active component of the renin-angiotensin-aldosterone system. Its exact role in renal vascular function is unclear. We therefore studied the effects of angiotensin(1-7) on the renal vasculature in vitro and in vivo.