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Elevated 12-lipoxygenase activity in the spontaneously hypertensive rat
1Division of Endocrinology, Department of Veteran's Affairs Medical Center, Sepulveda, California 91343, USA.
American Journal of Hypertension
|April 1, 1997
Summary
Elevated levels of 12(S)-hydroxyeicosatetraenoic acid (12-HETE) in spontaneously hypertensive rats (SHR) contribute to high blood pressure. Inhibiting the lipoxygenase (LO) pathway lowers blood pressure and vascular reactivity in these hypertensive models.
Area of Science:
- Biochemistry
- Physiology
- Pharmacology
Background:
- Lipoxygenase (LO) pathway inhibitors lower blood pressure in hypertensive rats.
- LO inhibition reduces vascular reactivity and calcium mobilization in smooth muscle cells.
Purpose of the Study:
- To investigate the relationship between elevated LO activity and hypertension.
- To compare 12(S)-hydroxyeicosatetraenoic acid (12-HETE) levels in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats.
Main Methods:
- Measurement of plasma and aortic smooth muscle 12-HETE levels in SHR and WKY rats at 4, 8, and 12 weeks.
- Administration of the LO inhibitor 5,8,11-eicosatriynoic acid (ETI) to 12-week-old SHR.
- Assessment of intracellular calcium levels in cultured vascular smooth muscle cells exposed to 12(S)-HETE and angiotensin II (AngII).
Main Results:
- 12-HETE levels were significantly elevated in SHR compared to WKY rats across all ages.
- ETI administration reduced systolic blood pressure in 12-week-old SHR.
- 12(S)-HETE pretreatment potentiated AngII-induced intracellular calcium levels in vascular smooth muscle cells.
Conclusions:
- Elevated LO products, specifically 12-HETE, may contribute to hypertension in SHR.
- LO products may influence vascular tone by altering intracellular calcium signaling pathways.
- Targeting the LO pathway could be a therapeutic strategy for hypertension.