We have investigated the role of cAMP in nitric oxide (NO)-and prostanoid-independent
vascular relaxations evoked by acetylcholine (ACh) in isolated arteries and perfused ear …

It is becoming increasingly evident that electrical signaling via gap junctions plays a central
role in the physiological control of vascular tone via two related mechanisms (1) the …

We have investigated the role of cAMP in NO-and prostanoid-independent relaxations that
are widely attributed to an endothelium-derived hyperpolarizing factor (EDHF). Under …

We have compared the mechanisms that contribute to endothelium-derived hyperpolarizing
factor (EDHF)-type responses induced by ACh and the Ca2+ ionophore A-23187 in the …

We have compared the contributions of gap junctional communication and chemical
signaling via H2O2 to NO-independent relaxations evoked by the Ca2+ ionophore A23187 …

The endothelium-dependent relaxation caused by acetylcholine (ACh) in rabbit aorta
segments was reduced by the nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine methyl …

Although an endothelium-derived hyperpolarizing factor (EDHF) has often been
hypothesized to underpin vascular relaxations that are independent of nitric oxide (NO) and …

NO-and prostanoid-independent relaxations are generally assumed to be mediated by an
endothelium-derived hyperpolarizing factor (EDHF) that has been postulated to be an …

The release of endothelium‐derived relaxing factors, such as nitric oxide (NO), is dependent
on an increase in intracellular calcium levels ([Ca2+] i) within endothelial cells. Endothelial …

In skeletal muscle arterioles, the pathway leading to non-nitric oxide (NO), non-
prostaglandin-mediated endothelium-derived hyperpolarizing factor (EDHF)-type dilations is …