Key Points
- To evaluate differences in mitogen-activated protein (MAP) kinase activation and signaling regulation between vascular smooth muscle cells of spontaneously hypertensive rats and normotensive controls.
- Stimulated early-passage vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats with angiotensin II (100 nmol/L) or PDGF-BB (10 ng/mL).
- Assessed MAP kinase activity using in-gel kinase assays and Western blot analysis, and examined calcium dependence via intracellular Ca2+ chelation with BAPTA.
- Inactivation of MAP kinase following angiotensin II stimulation occurred more rapidly in SHR VSMCs than in WKY VSMCs.
- Intracellular Ca2+ chelation with BAPTA inhibited maximal angiotensin II-induced MAP kinase activity by 95% in SHR VSMCs compared to 50% in WKY VSMCs.
- Stimulation with PDGF-BB revealed no differences in MAP kinase activity between SHR and WKY VSMCs.
Structured PICO
PPopulationEarly-passage spontaneously hypertensive rat (SHR) and Wistar-Kyoto (WKY) vascular smooth muscle cells (VSMCs)
IInterventionStimulation with angiotensin II (Ang II, 100 nmol/L) or platelet-derived growth factor-BB (PDGF-BB, 10 ng/mL)
CComparatorWKY VSMCs (normotensive control) compared to SHR VSMCs
OOutcomeMAP kinase activity measured by in-gel kinase assays and Western blot analysissurrogate
Angiotensin II-mediated MAP kinase activation exhibits distinct, Ca2+-dependent regulation in spontaneously hypertensive rat vascular smooth muscle cells, defining a hypertensive signal transduction phenotype.