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GPER Mediates Functional Endothelial Aging in Renal Arteries
Matthias R Meyer1, Thomas Rosemann, Matthias Barton
1Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Pharmacology
|July 14, 2017
Summary
Aging impairs renal artery function by increasing oxidative stress. The G-protein coupled estrogen receptor (GPER) is key to this age-related decline, as blocking its activity preserves artery function in older mice.
Area of Science:
- Cardiovascular Physiology
- Aging Research
- Renal Vascular Function
Background:
- Aging impairs renal artery function, leading to arterial stiffening and reduced vasodilation.
- This dysfunction is linked to increased reactive oxygen species (ROS) from NADPH oxidases (Nox).
- The role of G-protein coupled estrogen receptor (GPER) in age-related renal artery changes is unclear.
Purpose of the Study:
- To investigate the impact of aging and Nox activity on renal artery tone.
- To determine the contribution of GPER to age-dependent functional alterations in renal arteries.
Main Methods:
- Utilized wild-type and GPER-deficient (Gper-/-) mice at 4 and 24 months of age.
- Assessed renal artery tone and relaxation responses to acetylcholine and contractile agents.
- Employed a Nox inhibitor (gp91ds-tat) to evaluate the role of ROS.
Main Results:
- Aging significantly reduced endothelium-dependent, nitric oxide (NO)-mediated relaxations in wild-type mice.
- These age-related relaxations were preserved in aged Gper-/- mice.
- Nox inhibition restored relaxations in aged wild-type mice but not in Gper-/- mice, implicating Nox-derived ROS.
Conclusions:
- Basal GPER activity is essential for age-dependent impairment of renal artery relaxation.
- Nox-derived ROS are the primary cause of endothelial dysfunction in aging renal arteries.
- Targeting GPER signaling may mitigate endothelial aging and preserve kidney function.
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