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Vasopressin-induced vasoconstriction is dependent on MAPKerk1/2 phosphorylation
Jörn O Streefkerk1, Willem M H Hoogaars, Vincent M Christoffels
1The Department of Pharmacotherapy, Academic Medical Centre, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands. j.o.streefkerk@amc.uva.nl
Fundamental & Clinical Pharmacology
|January 30, 2004
Summary
Vasopressin causes vasoconstriction in rat aortas, partly through the mitogen-activated protein kinase (MAPK) ERK1/2 pathway. Inhibiting MAPK/ERK1/2 kinases reduced this vasopressin-induced vasoconstriction and phosphorylation.
Area of Science:
- Cardiovascular Physiology
- Molecular Signaling
Background:
- Vasopressin is a key regulator of blood pressure.
- The role of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) 1 and 2 (MAPK/ERK1/2) in vasopressin-mediated vasoconstriction is not fully understood.
Purpose of the Study:
- To investigate the involvement of the MAPK/ERK1/2 pathway in vasopressin-induced vasoconstriction in rat aorta.
Main Methods:
- Isolated rat thoracic aortae were used to measure vasopressin-induced vasoconstriction.
- Mek1/2 inhibitors (PD 98059 and U 0126) were employed to block MAPK/ERK1/2 kinase activity.
- Western blot analysis quantified MAPK/ERK1/2 phosphorylation.
Main Results:
- Vasopressin induced a concentration-dependent vasoconstriction.
- This vasoconstriction was significantly inhibited by Mek1/2 inhibitors.
- Vasopressin increased MAPK/ERK1/2 phosphorylation in a dose-dependent manner, which was prevented by Mek1/2 inhibitors.
Conclusions:
- The MAPK/ERK1/2 pathway plays a significant role in mediating vasopressin-induced vasoconstriction in rat aorta.
- Targeting the MAPK/ERK1/2 pathway may offer therapeutic potential for conditions involving abnormal vasopressin activity.