Key Points
- To determine whether oxygen-induced vasomotor responses in arterioles correspond to membrane potential changes in smooth muscle and endothelial cells.
- Performed intravital microscopy and intracellular microelectrode recordings with Lucifer yellow dye in cheek pouches of anesthetized male hamsters.
- Assessed smooth muscle and endothelial cell membrane potential (Em) and vessel diameter under low-PO2 (~20 Torr) and high-PO2 (~150 Torr) superfusion.
- Tested the effects of L-type Ca2+ channel blockers (diltiazem, 10 µM; nifedipine, 1 µM) and elevated extracellular K+ (55 mM) on electrical and mechanical responses.
- High-PO2 superfusion depolarized smooth muscle cells from -37 mV to -15 ± 1 mV and induced vasoconstriction from 55 ± 2 µm to 24 ± 2 µm, with vessel diameter cycling alongside smooth muscle membrane potential.
- Endothelial cell membrane potential averaged -36 mV at baseline and did not change during high-PO2 superfusion or vasomotion, despite depolarizing by 21 ± 2 mV under 55 mM extracellular K+.
- Superfusion with diltiazem or nifedipine completely abolished smooth muscle electrical and vasomotor responses to PO2 without blocking depolarization to elevated extracellular K+.
Structured PICO
PPopulationMale hamsters (cheek pouches prepared for intravital microscopy and intracellular recording)
IInterventionHigh-PO2 superfusion (approximately 150 Torr) and superfusion with diltiazem (10 microM) or nifedipine (1 microM)
CComparatorLow-PO2 superfusion (approximately 20 Torr)
OOutcomeChanges in membrane potential (Em) of smooth muscle cells (SMC) and endothelial cells (EC) and arteriolar diametersurrogate
Oxygen-induced vasoconstriction in arterioles is mediated by L-type calcium channels in smooth muscle cells without corresponding electrical activity in endothelial cells.