Key result
In human isolated small coronary arteries, relaxation to bradykinin is mediated by both nitric oxide and a K+-sensitive vasodilator mechanism, possibly endothelium-derived hyperpolarizing factor.
Population
Human isolated small coronary arteries
Comparison
Bradykinin in the presence of L-NOARG… vs Bradykinin without inhibitors or with different…
Design
Preclinical
Authors
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Highlights dual NO/EDHF pathways in human coronary arteries; leaves open the K+-sensitive factor's identity and in vivo role.
Endothelium-dependent relaxation to bradykinin in human small coronary arteries is mediated by both nitric oxide and a K+-sensitive vasodilator mechanism, likely EDHF.
Kemp et al. (1997) studied Human isolated small coronary arteries. L-NOARG, HbO, and high extracellular K+ was evaluated on Endothelium-dependent relaxation to bradykinin. In human isolated small coronary arteries, relaxation to bradykinin is mediated by both nitric oxide and a K+-sensitive vasodilator mechanism, possibly endothelium-derived hyperpolarizing factor.
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