ArticleBritish journal of pharmacology2004
Chronic treatment of male rats with daidzein and 17 beta-oestradiol induces the contribution of EDHF to endothelium-dependent relaxation.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- Unveiling the Pharmacological and Nanotechnological Facets of Daidzein: Present State-of-the-Art and Future Perspectives.Molecules (Basel, Switzerland) · 2023Review
- Review
- The Vascular Effects of Isolated Isoflavones-A Focus on the Determinants of Blood Pressure Regulation.Biology · 2021Review
- Potentiation of Acetylcholine-Induced Relaxation of Aorta in Male UC Davis Type 2 Diabetes Mellitus (UCD-T2DM) Rats: Sex-Specific Responses.Frontiers in physiology · 2021Article
- Alteration of Pressure-Induced Vasodilation in Aging and Diabetes, a Neuro-Vascular Damage.Frontiers in physiology · 2019Article
- Total Flavones ofEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Inducible endothelium-derived hyperpolarizing factor: role of the 15-lipoxygenase-EDHF pathway.Journal of cardiovascular pharmacology · 2013Review
- Vascular effects of phytoestrogens and alternative menopausal hormone therapy in cardiovascular disease.Mini reviews in medicinal chemistry · 2012Review
- Endothelium-derived hyperpolarizing factor in the brain: influence of sex, vessel size and disease state.Women's health (London, England) · 2011Article
- Potential approaches to enhance the effects of estrogen on senescent blood vessels and postmenopausal cardiovascular disease.Cardiovascular & hematological agents in medicinal chemistry · 2010Review
- Vascular pharmacology of epoxyeicosatrienoic acids.Advances in pharmacology (San Diego, Calif.) · 2010Review
- Research into Specific Modulators of Vascular Sex Hormone Receptors in the Management of Postmenopausal Cardiovascular Disease.Current hypertension reviews · 2009Article
- Analysis of the mechanisms underlying the endothelium-dependent antivasoconstriction of puerarin in rat aorta.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Arterial internal elastic lamina holes: relationship to function?Journal of anatomy · 2009Article
- Estrogenic compounds, estrogen receptors and vascular cell signaling in the aging blood vessels.Current medicinal chemistry · 2009Review
- Chronic ouabain treatment increases the contribution of nitric oxide to endothelium-dependent relaxation.Journal of physiology and biochemistry · 2008Article
- Simultaneous determination of multiple marker constituents in concentrated Gegen Tang granule by high performance liquid chromatography.Chinese medicine · 2007Article
- Acrolein induces vasodilatation of rodent mesenteric bed via an EDHF-dependent mechanism.Toxicology and applied pharmacology · 2006Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. We investigated the effect of chronic (7 days) treatment of male rats with the isoflavone daidzein (0.2 mg kg(-1) sc per day) or 17beta-oestradiol (0.1 mg kg(-1) sc per day) on the contribution of nitric oxide (NO), prostaglandins and endothelium-derived hyperpolarising factor (EDHF) to endothelium-dependent relaxation of isolated aortic rings. 2. The sensitivity and maximum relaxation to acetylcholine (ACh) were significantly greater in aortic rings from rats treated with daidzein or 17beta-oestradiol, in comparison to vehicle-treated rats. Inhibition of nitric oxide synthase with N-nitro-l-arginine (l-NOARG) abolished ACh-induced relaxation in the aortae from vehicle-treated rats, but only attenuated relaxation in aortae from daidzein or 17beta-oestradiol-treated rats. The presence of haemoglobin in addition to l-NOARG did not cause any further inhibition of relaxation. 3. The cyclooxygenase inhibitor indomethacin had no effect on endothelium-dependent relaxation in aortae from any treatment group. Charybdotoxin (ChTX), which blocks large-conductance calcium-activated potassium channels (BK(Ca)) and intermediate-conductance calcium-activated potassium channels (IK(Ca)), plus apamin, which blocks small-conductance calcium-activated potassium channels (SK(Ca)), but not iberiotoxin, which only blocks BK(Ca), attenuated endothelium-dependent relaxation of aortae from daidzein or 17beta-oestradiol-treated rats. Blockade of K(Ca) channels had no effect on the responses to ACh in aortae from vehicle-treated rats. In aortae from daidzein- or 17beta-oestradiol-treated rats, endothelium-dependent relaxation was also attenuated by inhibition of cytochrome P450 (CYP450) epoxygenase with 6-(2-propargylloxyphenyl)hexanoic acid (PPOH) or inhibition of K(IR) channels and Na(+)/K(+)-ATPase with barium and oubain, respectively. 4. This study demonstrates that endothelium-dependent relaxation of male rat aorta is normally entirely mediated by NO, whereas treatment with daidzein or 17beta-oestradiol stimulates a contribution from a non-NO, nonprostaglandin factor acting through the opening of SK(Ca) and IK(Ca) channels, and involving activation of Na/K-ATPase, K(IR) and CYP450 epoxygenase. This pattern of sensitivity to the tested inhibitors is consistent with the contribution of EDHF to relaxation. Thus, EDHF contributes to the enhanced endothelium-dependent relaxation that is observed after chronic treatment with the phytoestrogen daidzein or with 17beta-oestradiol.
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