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

An endothelium‐derived hyperpolarizing factor (EDHF) that is distinct from nitric oxide (NO)
and prostanoids has been widely hypothesized to hyperpolarize and relax vascular smooth …

The endothelium controls vascular tone adopting blood flow to tissue needs. It releases
chemical mediators [eg, nitric oxide (NO), prostaglandins (PG)] and exerts appreciable …

Nitric oxide (NO), together with prostacyclin (PGI2), mediates shear stress and endothelium-
dependent vasodilator-mediated vasorelaxation. In the presence of inhibition of NO …

Endothelium-derived hyperpolarizing factor (EDHF) was envisaged as a chemical entity
causing vasodilation by hyperpolarizing vascular smooth muscle (VSM) cells and distinct …

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 examined the effects of ouabain (1 mM), the gap junction inhibitors, 18α-
glycyrrhetinic acid (100 μM), N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2, 4-dichlorophenyl)-4 …

Endothelium‐dependent relaxations are attributed to the release of various factors, such as
nitric oxide, carbon monoxide, reactive oxygen species, adenosine, peptides and …

The endothelium-derived hyperpolarizing factor (EDHF) contributes critically to the
regulation of vascular tone. Its dependency on direct signaling through myoendothelial gap …