factor

(redirected from EDHF)
Also found in: Dictionary, Thesaurus, Medical, Financial, Acronyms, Encyclopedia.
Related to EDHF: Endothelin, EDRF

Factor

An event, circumstance, influence, or element that plays a part in bringing about a result.

A factor in a case contributes to its causation or outcome. In the area of Negligence law, the factors, or chain of causation, are important in determining whether liability ensues from a particular action done by the defendant.

factor

n. 1) a salesman who sells in his/her own name on behalf of others, taking a commission for services. 2) something that contributes to the result.

factor

1 a mercantile agent. An agent who is in the ordinary course of business entrusted with goods or documents of title representing goods with a view to their sale. A factor has a lien over goods entrusted to him; this lien covers any claims he may have against his principal arising out of the agency. Most factors will be mercantile agents (and have the powers of such) for the purposes of the Factors Act 1889. Under this Act, in certain circumstances a factor may pass a good title to goods entrusted to him.
2 an institution to whom a company assigns its book debts (see FACTORING).
3 in Scotland a landlord or superior's agent.
References in periodicals archive ?
Abbreviations: cga, chlorogenic acid; L-name, n[omega]-nitro-l-arginine methyl ester; Ach, acetylcholine; No, nitric oxide; NOS, NO synthase; COX, cyclooxygenase; EDHF, endothelium-derived hyperpolarizing factor.
Our results showed that administration of E2 directly into coronary arteries from sham-operated and gonadectomized rats caused rapid vasodilation by stimulating endothelial factors (NO, PGI2 and EDHF) production and opening potassium channels in all groups.
Our results showed that E2 stimulated the release of [PGI.sub.2] and EDHF, and activated potassium channels in all groups of normotensive rats.
However, the Crataegus treatment did affect neither the NO nor the EDHF components (Fig.
In the rat mesenteric artery, endothelium-dependent relaxations to ACh involve mainly a NO component (Furchgott and Zawadzki 1980) and an EDHF component (Chen et al.
In this report, we firstly investigated the direct dilative effect of total ginsenosides (TGS), the major bioactive constituents of ginseng (Attele et al., 1999; Furukawa et al., 2006), to the coronary artery in Langendorff rat heart preparation and then explored the potential roles of vasodilators NO, HO, CO, [PGI.sub.2] and EDHF in vasodilation induced by TGS in the rat hearts or human aortic endothelium cells (HAECs).
These inhibitors include: 100 [micro]M N(G)-nitro-L-arginine methyl ester (L-NAME, an NOS inhibitor) (Pabla and Curtis, 2007), 1.5 [micro]M protoporphyrin IX zinc (ZnPPIX, an HO inhibitor) (Sun et al., 2008), or 10 [micro]M 1-H-[1,2,4] oxadiaxolo[4,3-a] quinolalin-1-one [ODQ, a soluble guanylate cyclase (sGC) inhibitor] (Bolognesi et al., 2007), or 25 [micro]M indomethacin [a cyclooxygenase (COX) inhibitor to show the effect of [PGI.sub.2]] (Grbovic and Jovanovic, 1997), or 25 mM tetraethyl ammonium chloride (TEA, a potassium channel inhibitor to show the effect of EDHF) (Karamsetty et al., 1998).
Endothelium-dependent vasorelaxants, such as ACh, could also release an EDHF, which induces vasorelaxation by membrane hyperpolarization (Adeagbo and Triggle 1993).
Endothelium produces potent vasodilators, such as endothelium-derived relaxing factor (EDRF, NO), ptostacyclin and endothelium-derived hyperpolarizing factor (EDHF).
In those studies where the herbal extracts showed vasodilator effect on isolated aorta strips, as a result of investigating the underlying mechanism, some were suggested to be effective by releasing NO through endothelium, while several others were suggested to show their vasorelaxant effect not only via NO pathway, but also EDHF and/or prostacyclin pathways which play a significant role in the process.
Thus, in our study, EDHF mainly via activation of [K.sub.Ca] channels did not play a major role in aqueous hop extract-induced vasodilation of thoracic arterial rings from male and intact female rats.
In the present work, we describe an endothelium-dependent vasodilator effect of HSE in superior mesenteric artery rings of rats, through a mechanism dependent on release of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF).