|1.||He, Guo-Wei: 9 articles (01/2014 - 09/2002)|
|2.||Yang, Qin: 6 articles (01/2014 - 09/2002)|
|3.||Yim, Anthony P C: 6 articles (01/2007 - 09/2002)|
|4.||Shimokawa, Hiroaki: 5 articles (01/2015 - 05/2005)|
|5.||Goto, Kenichi: 5 articles (08/2009 - 07/2004)|
|6.||Buikema, Hendrik: 5 articles (02/2009 - 03/2003)|
|7.||Bełtowski, Jerzy: 4 articles (01/2014 - 05/2006)|
|8.||de Zeeuw, Dick: 4 articles (02/2009 - 03/2003)|
|9.||Fujii, Koji: 4 articles (02/2006 - 10/2002)|
|10.||Jamroz-Wiśniewska, Anna: 3 articles (01/2014 - 05/2006)|
07/01/2009 - "EDHF was likely the sole mediator responsible for the direct effects of LPC on U-46619-vasoconstriction, whereas the augmented vasoconstrictor responses following LPC washout may in part be related to an increase in ET-1, and a striking reduction in the bioavailability of NO. Our data suggest that in addition to reducing the accumulation of LPC to prevent ischemia-reperfusion (I/R) damage, efforts targeting an improved endothelium-dependent regulation of vascular tone could be an attractive approach to limit the cardiac damage induced by I/R."
01/01/2014 - "Pharmacological modulation of these channels during ischemia-reperfusion and hyperkalemic exposure show promising results on the preservation of NO and EDHF-mediated endothelial function, which suggests the potential of targeting endothelial K(+) and TRP channels for myocardial protection during cardiac surgery. "
01/01/2014 - "Hyperkalemic exposure and concurrent ischemia-reperfusion during cardioplegic intervention compromise NO and EDHF-mediated function and the impairment involves alterations of K(+) channels, that is, KATP and KCa, and Ca(2+)-permeable TRP channels in endothelial cells. "
04/01/2009 - "The preservation of EDHF responsiveness of PA after ischemia and reperfusion suggests an important role for this vasodilator under conditions when NOS is inhibited."
04/01/2009 - "The role of SK(Ca) and IK(Ca) channels in myogenic tone and endothelium-derived hyperpolarizing factor (EDHF) responsiveness was investigated under control conditions and after ischemia and reperfusion in parenchymal arterioles (PA) versus middle cerebral arteries (MCA). "
02/01/2015 - "The role of endothelium-derived hyperpolarizing factor (EDHF) in either the healthy circulation or in those with hypercholesterolemia is unknown. "
11/01/2005 - "Since ACh dilation in the arterioles of mice is mainly mediated via EDHF, we conclude that hypercholesterolemia does not alter EDHF release and efficacy. "
08/30/2004 - "Results indicate that hypercholesterolemia enhances endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in the rabbit renal artery and pioglitazon normalizes it without lowering serum lipid levels, and suggest that the maintenance of endothelial function by pioglitazon is related to the mechanisms for its anti-atheromatous activity."
05/01/2005 - "These results indicate that hypercholesterolemia alone minimally affects the EDHF-mediated relaxations, and diabetes mellitus significantly attenuated the responses, whereas their combination markedly attenuates the responses with a compensatory involvement of NO and a negative contribution of EDCF."
05/01/2005 - "Influence of diabetes mellitus, hypercholesterolemia, and their combination on EDHF-mediated responses in mice."
|3.||Cardiovascular Diseases (Cardiovascular Disease)
05/01/2005 - "The impact of dyslipidaemia (DL), a risk factor for cardiovascular diseases, on the nature and the efficacy of EDHF has not been evaluated yet. "
08/01/2009 - "A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases."
02/01/2009 - "Aging and cardiovascular diseases are associated with endothelial dysfunctions that can involve a decrease in NO bioavailability, alterations of EDHF-mediated responses and/or enhanced production of endothelium-derived contracting factors. "
07/01/1997 - "This could lead to the design of new therapies aimed at correcting the impairment of EDHF-mediated dilatation in a number of cardiovascular diseases."
06/01/2010 - "Together with other endothelium-dependent dilator pathways 'EDHF' hyperpolarization is compromised by cardiovascular disease, including hypertension. "
12/01/2006 - "To analyze gender related alterations in NO-, PGI(2)- and EDHF-dependent endothelial function in the thoracic aorta 7 and 42 days after myocardial infarction (MI). "
12/01/2005 - "These findings highlight the importance of EDHF impairment in development of endothelial dysfunction after myocardial infarction and the possibility of improving EDHF-mediated vasodilation with chronic ACE inhibitor therapy. "
12/01/2005 - "Improvement of EDHF by chronic ACE inhibition declines rapidly after withdrawal in rats with myocardial infarction."
12/01/2005 - "Long-term quinapril (8 months) resulted in markedly improved endothelium-dependent vasodilation in rats with myocardial infarction, which could be attributed to marked improvement in non-NO/prostanoid-mediated relaxation (ie, EDHF). "
12/01/2006 - "Functional alterations in NO, PGI2 and EDHF pathways in the aortic endothelium after myocardial infarction in rats."
|5.||Hypertension (High Blood Pressure)
10/01/2007 - "The aims of the present study were to evaluate the changes of endothelium-dependent dilatation of arteries in hypertension and the role of ADMA in NO- and EDHF-mediated vasodilatation. "
11/15/2004 - "The present study was designed to elucidate whether the conduction of vasomotor responses mediated by endothelium-derived hyperpolarizing factor (EDHF) in rat mesenteric arteries is altered during hypertension. "
03/01/1996 - "Another goal of this study was to evaluate whether this model of hypertension is accompanied by changes in the activity of endothelium-derived hyperpolarizing factor (EDHF). "
04/30/2015 - "In conclusion, an impairment in EDHF/H2S signaling occurs in earlier state of GC-induced hypertension in rats suggesting that counteracting this dysfunction may be beneficial to manage DEX-associated increase in blood pressure."
04/06/2012 - "Mutation or down-regulation of RGS2 in hypertension patients therefore may contribute to endothelial dysfunction and defective EDHF-dependent relaxation. "
|3.||Nitric Oxide (Nitrogen Monoxide)
|5.||Nitric Oxide Synthase (NO Synthase)
|6.||NG-Nitroarginine Methyl Ester (L-NAME)
|8.||Nicorandil (SG 75)
|10.||Type 1 Angiotensin Receptor
|1.||Angioplasty (Angioplasty, Transluminal)
|3.||Induced Heart Arrest (Cardioplegia)