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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
Published on: June 7, 2016
Angiotensin II type 2 receptor mediated angiotensin II and high glucose induced decrease in renal prorenin/renin
Ming He1, Lin Zhang, Ying Shao
1Department of Physiology and Pathophysiology, Fudan University, Shanghai Medical College, 138 Yi Xue Yuan Road, Shanghai 200032, China.
Molecular and Cellular Endocrinology
|November 3, 2009
Summary
High glucose and angiotensin II (Ang II) reduce prorenin/renin receptor [(P)RR] expression in diabetic kidneys. This reduction is mediated by the Ang II type 2 receptor (AT(2)R), not the AT(1)R.
Area of Science:
- Nephrology
- Endocrinology
- Molecular Biology
Background:
- The prorenin/renin receptor [(P)RR] is involved in the non-enzymatic functions of renin-angiotensin system components.
- (P)RR plays a role in diabetic nephropathy pathogenesis, but its regulatory mechanisms under hyperglycemia remain unclear.
Purpose of the Study:
- To investigate the regulation of (P)RR expression in the kidneys of streptozotocin (STZ)-induced diabetic rats and cultured rat renal glomerular mesangial cells (MCs) under hyperglycemic conditions.
Main Methods:
- Studied (P)RR mRNA levels in STZ-diabetic rats and cultured MCs.
- Measured plasma and renal angiotensin II (Ang II) levels.
- Utilized AT(2)R antagonist (PD123319) and AT(1)R antagonist (losartan) to assess receptor involvement.
- Examined the effects of Ang II and high glucose on (P)RR expression in MCs.
Main Results:
- STZ-induced diabetic rats showed decreased renal (P)RR mRNA levels, increased Ang II, and increased AT(2)R mRNA.
- In cultured MCs, Ang II and high glucose significantly reduced (P)RR expression.
- The inhibitory effects of Ang II and high glucose on (P)RR were blocked by the AT(2)R antagonist PD123319 but not the AT(1)R antagonist losartan.
Conclusions:
- Activation of the AT(2)R, not AT(1)R, mediates the reduction in (P)RR expression induced by Ang II and high glucose.
- These findings highlight the role of AT(2)R in regulating (P)RR in diabetic kidney disease.
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