Key Points
- To examine how the vascular endothelium modulates sympathetic nerve-mediated vasoconstriction and noradrenaline release in isolated rat tail arteries.
- Perfused isolated rat tail artery segments at a constant flow rate and applied transmural electrical stimulation in the presence and absence of intact endothelium.
- Simultaneously measured changes in perfusion pressure and quantified noradrenaline release via high-performance liquid chromatography with electrochemical detection.
- Assessed vascular and neurochemical responsiveness during exposure to pharmacological modulators, including L-NAME, methylene blue, carbachol, and angiotensin II.
- Removal of the endothelium increased both basal and stimulation-evoked noradrenaline release and perfusion pressure, identifying an endogenous prejunctional inhibitory influence.
- Inhibition of nitric oxide synthase with L-NAME or soluble guanylyl cyclase with methylene blue enhanced stimulation-induced perfusion pressure without altering noradrenaline release in endothelium-intact arteries.
- Carbachol reduced noradrenaline release and perfusion pressure increases, whereas angiotensin II potentiated vasoconstrictor responses in an endothelium-dependent manner.
Structured PICO
PPopulationIsolated and perfused segments of the rat tail artery
IInterventionEndothelium removal and perfusion with various drugs (L-NAME, methylene blue, carbachol, Angiotensin II)
CComparatorArteries with intact endothelium and absence of drugs
OOutcomeNoradrenaline release and changes in perfusion pressuresurrogate
The study demonstrates that sympathetic vasoconstriction in the rat tail artery is modulated by three distinct endothelial factors: nitric oxide, an endothelium-derived contracting factor, and an endothelium-derived inhibitory factor.