Loss of biphasic effect on Na/K-ATPase activity by angiotensin II involves defective angiotensin type 1 receptor-nitric oxide signaling. [electronic resource]
Producer: 20081231Description: 1099-105 p. digitalISSN:- 1524-4563
- Angiotensin II -- pharmacology
- Animals
- Antihypertensive Agents -- pharmacology
- Antioxidants -- pharmacology
- Benzimidazoles -- pharmacology
- Biphenyl Compounds
- Blood Pressure -- drug effects
- Buthionine Sulfoximine -- pharmacology
- Cyclic GMP -- metabolism
- Cyclic N-Oxides -- pharmacology
- Enzyme Inhibitors -- pharmacology
- Focal Adhesion Kinase 2 -- metabolism
- Hypertension, Renal -- chemically induced
- Kidney Tubules, Proximal -- drug effects
- Male
- Mitogen-Activated Protein Kinases -- metabolism
- Nitric Oxide -- metabolism
- Oxidative Stress -- drug effects
- Rats
- Rats, Sprague-Dawley
- Receptor, Angiotensin, Type 1 -- metabolism
- Signal Transduction -- drug effects
- Sodium-Hydrogen Exchanger 3
- Sodium-Hydrogen Exchangers -- metabolism
- Sodium-Potassium-Exchanging ATPase -- metabolism
- Spin Labels
- Tetrazoles -- pharmacology
- Vasoconstrictor Agents -- pharmacology
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Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
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