Abstract
Introduction: systemic hypertension (SH) involving endothelial dysfunction contributes to immune complex-mediated glomerulonephritis (ICGN). Objective, we demonstrate a relationship between ICGN and SH by analyzing vascular reactivity in renal aortic rings. Methods: 48 male Wistar rats were divided into four groups: (a) control (C); (b) injected with bovine serum albumin (BSA); (c) receiving 200 mg/L NAME (an analog of arginine that inhibits NO production) in drinking water; and (d) receiving BSA and 200 mg/L NAME. Rats were pre-immunized subcutaneously with BSA and Freund’s adjuvant. After 10 days, groups (b) and (c) received 1 mg/mL of BSA in saline intravenous (IV) daily for 35 days. The urine of 24 h was measured at days 0, 15, 30 and 45. Results: vascular reactivity to norepinephrine (NE), acetylcholine (Ach) and NAME were tested. Creatinine clearance, vasodilatation, eNOS and elastic fibers were diminished (p ≤ 0.001). Blood pressure, vasoconstriction, iNOS were increased, and glomerular alterations were observed in groups (b), (c) and (d) when compared to group (a) (p ≤ 0.001). Conclusions: SH contributes to the development of progressive renal disease in ICGN. Alterations of the vascular reactivity are mediated by the endothelium in the renal aorta. Thus, the endothelium plays a determinant role in the production of vasoactive substances such as NO during this process.
Highlights
Renal diseases represent a serious worldwide problem and their study in experimental models constitutes an important tool to understand their pathogenesis and their natural evolution [1].It is nowadays accepted that the majority of glomerulonephritis occurring in humans has an immunologic origin [2]
The results show that the downregulated expression of eNOS and the increase in iNOS expression in the endothelium of the bovine serum albumin (BSA), NAME- and BSA + NAME-treated groups can favor
An increase in the expansion of mesangial cells can be the reason why, when mesangial function is impaired, deposits derived from immune complexes persist, and our results show an increase in expansion of the mesangium in the BSA, NAME and BSA + NAME groups
Summary
Renal diseases represent a serious worldwide problem and their study in experimental models constitutes an important tool to understand their pathogenesis and their natural evolution [1]. It is nowadays accepted that the majority of glomerulonephritis occurring in humans has an immunologic origin [2]. This hypothesis is supported by the presence of deposits of immune complexes with complement protein in renal biopsies and by the presence of inflammatory cells and electron-dense immune deposits [3]. Clinical and laboratory findings have demonstrated the presence of. Res. Public Health 2018, 15, 1164; doi:10.3390/ijerph15061164 www.mdpi.com/journal/ijerph
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