We investigated whether angiotensin II (AII) peptide is induced in the rat kidney under endotoxemic conditions. Immunohistochemistry revealed strong AII-like immunoreactivity in the renal tubules of rats given high-dose lipopolysaccharide (LPS; 1000 microg/kg) intraperitoneally (i.p.). AII-like immunoreactivity in renal tubules was slight at 1h after the LPS injection, but marked at 3 h. There were few signals in the kidney in saline-injected control rats. When injected at 0.1, 10, or 1000 microg/kg i.p., LPS-induced a dose-related increase in AII-like immunoreactivity in renal tubules that was unaffected by treatment with the prostaglandin-synthesis blocker indomethacin. ELISA measurement of the AII concentration in the whole kidney supported the above findings. These results suggest that systemically administered LPS induces AII peptide expression in renal tubules by a prostaglandin-independent mechanism.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.peptides.2005.03.057DOI Listing

Publication Analysis

Top Keywords

renal tubules
20
aii-like immunoreactivity
12
immunoreactivity renal
12
aii peptide
8
1000 microg/kg
8
renal
5
tubules
5
systemic administration
4
administration lipopolysaccharide
4
lipopolysaccharide upregulates
4

Similar Publications

LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice.

J Transl Med

January 2025

Department of Basic Medical Sciences, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310058, China.

Background: The partial epithelial-mesenchymal transition (EMT) is emerging as a significant mechanism in diabetic nephropathy (DN). LOX is a copper amine oxidase conventionally thought to act by crosslinking collagen. However, the role of LOX in partial EMT and fibrotic progression in diabetic nephropathy has not been investigated experimentally.

View Article and Find Full Text PDF

High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux.

Hum Cell

January 2025

Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.

Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.

View Article and Find Full Text PDF

Backgrounds: The pathophysiology of nephrolithiasis is complex, influenced by both environmental and genetic factors. Calcium is the most prevalent metabolite present in the stone matrix. Stimulating the basolateral calcium sensing receptor (CASR) in the renal tubules leads to an increase in claudin-14 expression, reducing paracellular calcium permeability and increasing urinary Ca excretion.

View Article and Find Full Text PDF

SARS-Cov-2 is a corona virus that causes COVID-19 disease, a viral infection responsible for the pandemic decreed by the World Health Organization in March 2020. Angiotensin-converting enzyme 2 (ACE-2) functions as the main receptor for SARS-Cov-2. The study aimed to detect the expression of ACE-2 in the gastrointestinal tract, kidney, and lung in the rhesus monkeys and squirrel monkeys.

View Article and Find Full Text PDF

The role played by anionic channels in diabetic kidney disease (DKD) is not known. Chloride channel accessory 1 (CLCA1) facilitates the activity of TMEM16A (Anoctamin-1), a Ca2+-dependent Cl- channel. We examined if CLCA1/TMEM16A had a role in DKD.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!