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Decreased blood pressure in NOX1-deficient mice
Gaetan Gavazzi1, Botond Banfi, Christine Deffert
1Department of Rehabilitation and Geriatrics, Geneva Medical Faculty, 1211 Geneva 4, Switzerland.
Abstract:
To understand the role of the superoxide-generating NADPH oxidase NOX1 in the vascular system, we have generated NOX1-deficient mice. NOX1-deficient mice had a moderately decreased basal blood pressure. In response to angiotensin II they showed an almost complete loss of the sustained blood pressure response, while the initial increase was conserved. NOX1-deficient mice showed a marked reduction in aortic media hypertrophy. Angiotensin II-induced smooth muscle cell proliferation was conserved, but there was a marked decrease in extracellular matrix accumulation. Our results establish a role for NOX1 in blood pressure regulation and vascular angiotensin II response.
Insights
Mice lacking NADPH oxidase NOX1 showed reduced blood pressure and impaired responses to angiotensin II, indicating NOX1
Area of Science:
- Vascular Biology
- Biochemistry
- Physiology
Background:
- NADPH oxidase NOX1 generates superoxide, a key signaling molecule.
- The role of NOX1 in the vascular system is not fully understood.
Purpose of the Study:
- To investigate the function of NOX1 in blood pressure regulation and vascular responses to angiotensin II.
Main Methods:
- Generated NOX1-deficient mice.
- Measured basal blood pressure.
- Assessed blood pressure response to angiotensin II infusion.
- Analyzed aortic media hypertrophy and extracellular matrix accumulation.
Main Results:
- NOX1-deficient mice exhibited moderately decreased basal blood pressure.
- A significant reduction in the sustained blood pressure response to angiotensin II was observed.
- Aortic media hypertrophy was markedly reduced in NOX1-deficient mice.
- Extracellular matrix accumulation in response to angiotensin II was significantly decreased, while smooth muscle cell proliferation was conserved.
Conclusions:
- NOX1 plays a crucial role in maintaining basal blood pressure.
- NOX1 is essential for the sustained vascular response to angiotensin II.
- NOX1 influences vascular remodeling by regulating extracellular matrix deposition.
