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      Endothelium-derived hyperpolarizing factor mediates bradykinin-stimulated tissue plasminogen activator release in humans.

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          Abstract

          Bradykinin (BK) stimulates tissue plasminogen activator (t-PA) release from human endothelium. Although BK stimulates both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) release, the role of EDHF in t-PA release remains unexplored. This study sought to determine the mechanisms of BK-stimulated t-PA release in the forearm vasculature of healthy human subjects.

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          Prognostic value of coronary vascular endothelial dysfunction.

          Julian P J Halcox, William H Schenke, Gloria Zalos … (2002)
          Whether patients at increased risk can be identified from a relatively low-risk population by coronary vascular function testing remains unknown. We investigated the relationship between coronary endothelial function and the occurrence of acute unpredictable cardiovascular events (cardiovascular death, myocardial infarction, stroke, and unstable angina) in patients with and without coronary atherosclerosis (CAD). We measured the change in coronary vascular resistance (DeltaCVR) and epicardial diameter with intracoronary acetylcholine (ACh, 15 micro g/min) to test endothelium-dependent function and sodium nitroprusside (20 micro g/min) and adenosine (2.2 mg/min) to test endothelium-independent vascular function in 308 patients undergoing cardiac catheterization (132 with and 176 without CAD). Patients underwent clinical follow-up for a mean of 46+/-3 months. Acute vascular events occurred in 35 patients. After multivariate analysis that included CAD and conventional risk factors for atherosclerosis, DeltaCVR with ACh (P=0.02) and epicardial constriction with ACh (P=0.003), together with increasing age, CAD, and body mass index, were independent predictors of adverse events. Thus, patients in the tertile with the best microvascular responses with ACh and those with epicardial dilation with ACh had improved survival by Kaplan-Meier analyses in the total population, as did those in the subset without CAD. Similar improvement in survival was also observed when all adverse events, including revascularization, were considered. Endothelium-independent responses were not predictive of outcome. Epicardial and microvascular coronary endothelial dysfunction independently predict acute cardiovascular events in patients with and without CAD, providing both functional and prognostic information that complements angiographic and risk factor assessment.
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            Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy.

            J. Lambeth (2007)
            Reactive oxygen species (ROS) are considered to be chemically reactive with and damaging to biomolecules including DNA, protein, and lipid, and excessive exposure to ROS induces oxidative stress and causes genetic mutations. However, the recently described family of Nox and Duox enzymes generates ROS in a variety of tissues as part of normal physiological functions, which include innate immunity, signal transduction, and biochemical reactions, e.g., to produce thyroid hormone. Nature's "choice" of ROS to carry out these biological functions seems odd indeed, given its predisposition to cause molecular damage. This review describes normal biological roles of Nox enzymes as well as pathological conditions that are associated with ROS production by Nox enzymes. By far the most common conditions associated with Nox-derived ROS are chronic diseases that tend to appear late in life, including atherosclerosis, hypertension, diabetic nephropathy, lung fibrosis, cancer, Alzheimer's disease, and others. In almost all cases, with the exception of a few rare inherited conditions (e.g., related to innate immunity, gravity perception, and hypothyroidism), diseases are associated with overproduction of ROS by Nox enzymes; this results in oxidative stress that damages tissues over time. I propose that these pathological roles of Nox enzymes can be understood in terms of antagonistic pleiotropy: genes that confer a reproductive advantage early in life can have harmful effects late in life. Such genes are retained during evolution despite their harmful effects, because the force of natural selection declines with advanced age. This review discusses some of the proposed physiologic roles of Nox enzymes, and emphasizes the role of Nox enzymes in disease and the likely beneficial effects of drugs that target Nox enzymes, particularly in chronic diseases associated with an aging population.
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              Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors.

              Doris Campbell, D Gebremedhin, Jonathan D Harder … (1996)
              Endothelial cells release several compounds, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF), that mediate the vascular effects of vasoactive hormones. The identity of EDHF remains unknown. Since arachidonic acid causes endothelium-dependent relaxations of coronary arteries through its metabolism to epoxyeicosatrienoic acids (EETs) by cytochrome P450, we wondered if the EETs represent EDHFs. Precontracted bovine coronary arteries relaxed in an endothelium-dependent manner to methacholine. The cytochrome P450 inhibitors, SKF 525A and miconazole, significantly attenuated these relaxations. They were also inhibited by tetraethylammonium (TEA),an inhibitor of Ca2+-activated K+ channels, and by high [K+]0 (20 mmol/L). Methacholine also caused hyperpolarization of coronary smooth muscle (-27 +/- 3.9 versus -40 +/- 5.1 mV), which was completely blocked by SKF 525A and miconazole. In vessels prelabeled with [3H] arachidonic acid, methacholine stimulated the release of 6-ketoprostaglandin F1alpha, 12-HETE, and the EETs. Arachidonic acid relaxed precontracted coronary arteries, which were also blocked by TEA, charybdotoxin, another Ca2+-activated K+ channel inhibitor, and high [K+]0. 14,15-EET, 11,12-EET, 8,9-EET, and 5,6-EET relaxed precontracted coronary vessels (EC50, 1 X 10(-6) mol/L). The four regioisomers were equally active. TEA, charybdotoxin, and high [K+]0 attenuated the EET relaxations. 11,12-EET hyperpolarized coronary smooth muscle cells from -37 +/- 0.2 to -59 +/- 0.3 mV. In the cell-attached mode of patch clamp, both 14,15-EET and 11,12-EET increased the open-state probability of a Ca2+-activated K+ channel in coronary smooth muscle cells. This effect was blocked by TEA and charybdotoxin. These data support the hypothesis that the EETs are EDHFs.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J. Vasc. Res.
                Title: Journal of vascular research
                Publisher: S. Karger AG
                ISSN (Electronic): 1423-0135
                ISSN (Print): 1018-1172
                Publication date (Electronic): 2014
                Volume: 51
                Issue: 3
                Affiliations
                [1 ] Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Ga., USA.
                Article
                Publisher Item ID: 000362666 Mid ID: NIHMS584572
                DOI: 10.1159/000362666
                PMC ID: 4149839
                PubMed ID: 24925526
                SO-VID: 240af767-580d-4566-ad3a-3db027c3f0a4
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