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  • 1
    Online Resource
    Online Resource
    Overexpression of CuZn-SOD Prevents Lipopolysaccharide-Induced Endothelial Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Stroke Vol. 35, No. 8 ( 2004-08), p. 1963-1967
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 8 ( 2004-08), p. 1963-1967
    Abstract: Background and Purpose— Inflammation is thought to be a major contributor to carotid artery disease. Lipopolysaccharide (LPS) activates inflammatory mechanisms thought to contribute to endothelial dysfunction by mechanisms that are not well defined. The goal of this study was to determine whether overexpression of CuZn-SOD protects against LPS-induced increases in superoxide and endothelial dysfunction. Methods— Carotid arteries from CuZn-SOD transgenic (SOD-Tg) and nontransgenic (non-Tg) littermates were examined in vitro. Superoxide levels were measured using lucigenin-enhanced chemiluminescence. Results— In non-Tg mice, LPS (0.5 μg/mL for 22 hours) produced marked impairment of vasorelaxation in response to the endothelium-dependent dilator acetylcholine (ACh). For example, 100 μmol/L ACh relaxed carotid arteries from non-Tg mice by 86±6% and 38±8% after treatment with vehicle and LPS, respectively. In contrast, LPS did not significantly impair responses of carotid artery to ACh in SOD-Tg mice, and LPS had no effect on relaxation responses to the endothelium-independent dilator nitroprusside in carotid artery from non-Tg or SOD-Tg mice. LPS-induced increases in superoxide, as measured using lucigenin-enhanced chemiluminescence, were higher in vessels from non-Tg mice than from SOD-Tg mice. Conclusions— These results indicate that LPS increases superoxide and impairs endothelium-dependent relaxation. Overexpression of the CuZn isoform of SOD effectively prevents LPS-induced oxidative stress and endothelial dysfunction in the carotid artery.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.0000132764.06878.c5
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1467823-8
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  • 2
    Online Resource
    Online Resource
    Increased Superoxide and Vascular Dysfunction in CuZnSOD-Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Circulation Research Vol. 91, No. 10 ( 2002-11-15), p. 938-944
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 91, No. 10 ( 2002-11-15), p. 938-944
    Abstract: Increased superoxide is thought to play a major role in vascular dysfunction in a variety of disease states. Superoxide dismutase (SOD) limits increases in superoxide; however, the functional significance of selected isoforms of SOD within the vessel wall are unknown. We tested the hypothesis that selective loss of CuZnSOD results in increased superoxide and altered vascular responsiveness in CuZnSOD-deficient (CuZnSOD −/− ) mice compared with wild-type (CuZnSOD +/+ ) littermates. Total SOD activity was reduced ( P 〈 0.05) by approximately 60% and CuZnSOD protein was absent in aorta from CuZnSOD −/− as compared with wild-type mice. Vascular superoxide levels, measured using lucigenin (5 μmol/L)-enhanced chemiluminescence and hydroethidine (2 μmol/L)-based confocal microscopy, were increased (approximately 2-fold; P 〈 0.05) in CuZnSOD −/− mice as compared with wild-type mice. Relaxation of the carotid artery in response to acetylcholine and authentic nitric oxide was impaired ( P 〈 0.05) in CuZnSOD −/− mice. For example, maximal relaxation to acetylcholine (100 μmol/L) was 50±6% and 69±5% in CuZnSOD −/− and wild-type mice, respectively. Contractile responses of the carotid artery were enhanced ( P 〈 0.05) in CuZnSOD −/− mice in response to phenylephrine and serotonin, but not to potassium chloride or U46619. In vivo, dilatation of cerebral arterioles (baseline diameter=31±1 μm) to acetylcholine was reduced by approximately 50% in CuZnSOD −/− mice as compared with wild-type mice ( P 〈 0.05). These findings provide the first direct insight into the functional importance of CuZnSOD in blood vessels and indicate that this specific isoform of SOD limits increases in superoxide under basal conditions. CuZnSOD-deficiency results in altered responsiveness in both large arteries and microvessels.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000043280.65241.04
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 1467838-X
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  • 3
    Online Resource
    Online Resource
    Suppressed impact of nitric oxide on renal arteriolar function in rats with chronic heart failure
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Renal Physiology Vol. 276, No. 1 ( 1999-01-01), p. F79-F87
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 276, No. 1 ( 1999-01-01), p. F79-F87
    Abstract: We performed experiments to test the hypothesis that experimental heart failure (HF) is associated with altered nitric oxide (NO)-dependent influences on the renal microvasculature, including diminished modulation of constrictor responses to ANG II. Eight to ten weeks after inducing HF in rats by coronary artery ligation, we administered enalaprilat to suppress ANG II synthesis and studied renal arteriolar function using the in vitro blood-perfused juxtamedullary nephron technique. In kidneys from sham-operated rats, NO synthase inhibition [100 μM N ω -nitro-l-arginine (l-NNA)] reduced afferent arteriolar diameter by 4.1 ± 0.6 μm and enhanced ANG II responsiveness (10 nM ANG II decreased afferent diameter by 10.1 ± 1.4 μm before and 12.8 ± 1.6 μm duringl-NNA treatment; P 〈 0.05). In kidneys from HF rats,l-NNA did not alter afferent arteriolar baseline diameter or ANG II responsiveness (10 nM ANG II decreased diameter by 12.5 ± 1.5 μm before and 12.5 ± 2.3 μm during l-NNA). The effects of l-NNA on efferent arteriolar function were also abated in HF rats. In renal cortex of HF rats, NO synthase activity was decreased by 63% and superoxide dismutase activity was diminished by 39% relative to tissue from sham-operated rats. Urinary nitrate/nitrite excretion was also reduced in HF rats. Thus both diminished synthesis and augmented degradation are likely to contribute to a decreased renal microvascular impact of endogenous NO during chronic HF, the consequences of which include loss of NO-dependent modulation of ANG II-induced vasoconstriction.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1999.276.1.F79
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477287-5
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  • 4
    Online Resource
    Online Resource
    L-Arginine Does Not Restore Dilatation of the Basilar Artery during Diabetes Mellitus
    SAGE Publications ; 1996
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 16, No. 3 ( 1996-05), p. 500-506
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 16, No. 3 ( 1996-05), p. 500-506
    Abstract: The goal of this study was to test the hypothesis that administration of L-arginine, a substrate for the synthesis of nitric oxide, restores endothelium-dependent dilatation of the basilar artery during diabetes mellitus. We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic (streptozotocin; 50–60 mg/kg i.p.) rats in response to endothelium-dependent agonists (acetylcholine and bradykinin) and an endothelium-independent agonist (nitroglycerin) before and during application of L-arginine. Topical application of acetylcholine (1.0 and 10 μ M) and bradykinin (1.0 and 10 μ M) produced dilatation in nondiabetic rats of the basilar artery which was impaired in diabetic rats. Topical application of nitroglycerin (0.1 and 1.0 μ M) produced similar dilatation of the basilar artery in nondiabetic and diabetic rats. Topical application of L-arginine (0.1 and 3 m M) did not enhance dilatation of the basilar artery in response to acetylcholine and bradykinin in diabetic rats. Thus, impairment of dilatation of the basilar artery in diabetic rats in response to acetylcholine and bradykinin appears to be related to a mechanism unrelated to the availability of L-arginine for nitric oxide synthase.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/00004647-199605000-00017
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1996
    detail.hit.zdb_id: 2039456-1
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  • 5
    Online Resource
    Online Resource
    Sex differences in the vascular function and related mechanisms: role of 17β-estradiol
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 315, No. 6 ( 2018-12-01), p. H1499-H1518
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 315, No. 6 ( 2018-12-01), p. H1499-H1518
    Abstract: The incidence of cardiovascular disease (CVD) is lower in premenopausal women but increases with age and menopause compared with similarly aged men. Based on the prevalence of CVD in postmenopausal women, sex hormone-dependent mechanisms have been postulated to be the primary factors responsible for the protection from CVD in premenopausal women. Recent Women’s Health Initiative studies, Cochrane Review studies, the Early Versus Late Intervention Trial with Estradiol Study, and the Kronos Early Estrogen Prevention Study have suggested that beneficial effects of hormone replacement therapy (HRT) are seen in women of 〈 60 yr of age and if initiated within 〈 10 yr of menopause. In contrast, the beneficial effects of HRT are not seen in women of 〉 60 yr of age and if commenced after 10 yr of menopause. The higher incidence of CVD and the failure of HRT in postmenopausal aged women could be partly associated with fundamental differences in the vascular structure and function between men and women and in between pre- and postmenopausal women, respectively. In this regard, previous studies from human and animal studies have identified several sex differences in vascular function and associated mechanisms. The female sex hormone 17β-estradiol regulates the majority of these mechanisms. In this review, we summarize the sex differences in vascular structure, myogenic properties, endothelium-dependent and -independent mechanisms, and the role of 17β-estradiol in the regulation of vascular function.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00194.2018
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Effect of Chronic Alcohol Consumption on Responses of Cerebral Arterioles
    Wiley ; 1996
    In:  Alcoholism: Clinical and Experimental Research Vol. 20, No. 3 ( 1996-05), p. 538-542
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 20, No. 3 ( 1996-05), p. 538-542
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.1996.20.issue-3
    DOI: 10.1111/j.1530-0277.1996.tb01089.x
    Language: English
    Publisher: Wiley
    Publication Date: 1996
    detail.hit.zdb_id: 2046886-6
    detail.hit.zdb_id: 3167872-5
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Essential role of interleukin-6 in angiotensin-II-induced endothelial dysfunction
    Elsevier BV ; 2006
    In:  Vascular Pharmacology Vol. 45, No. 3 ( 2006-09), p. e6-
    Details
    In: Vascular Pharmacology, Elsevier BV, Vol. 45, No. 3 ( 2006-09), p. e6-
    Type of Medium: Online Resource
    ISSN: 1537-1891
    URL: Article
    DOI: 10.1016/j.vph.2006.08.066
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2006
    detail.hit.zdb_id: 2089264-0
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    Acute Effects of Ethanol on Responses of Cerebral Arterioles
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Stroke Vol. 26, No. 11 ( 1995-11), p. 2097-2102
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 26, No. 11 ( 1995-11), p. 2097-2102
    Abstract: Background and Purpose Previous studies have suggested that acute exposure of large peripheral arteries to ethanol impairs endothelium-dependent relaxation. The goal of the present study was to determine the acute effects of ethanol exposure on responses of cerebral resistance arterioles in vivo. Methods We prepared a cranial window in rats to expose the cerebral (pial) microcirculation. We measured the diameter of pial arterioles in vivo in response to agonists that presumably stimulate the synthesis/release of nitric oxide from the endothelium (ADP, acetylcholine, and histamine) or neurons ( N -methyl- d -aspartate [NMDA]) before and after topical application of various concentrations of ethanol added to the cerebrospinal fluid (20, 40, 60, 80, and 100 mmol/L). In addition, we examined responses of pial arterioles to nitroglycerin before and 1 hour after topical application of ethanol. Results Before application of ethanol, ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related dilatation of pial arterioles. Application of the various concentrations of ethanol did not alter the baseline diameter of pial arterioles. However, application of 80 and 100 mmol/L ethanol inhibited dilatation of pial arterioles in response to agonists that stimulate the synthesis/release of nitric oxide. Dilatation of pial arterioles in response to nitroglycerin was not altered by application of ethanol. Conclusions The findings of the present study suggest that acute exposure of cerebral arterioles to modest-to-moderate concentrations of ethanol (20 to 60 mmol/L) does not alter responses of cerebral arterioles. In contrast, exposure of cerebral arterioles to higher concentrations of ethanol (80 and 100 mmol/L) can produce specific impairment of dilatation to agonists that stimulate the synthesis/release of nitric oxide from endothelium and neurons.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.26.11.2097
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
    detail.hit.zdb_id: 1467823-8
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  • 9
    Online Resource
    Online Resource
    Vascular Protection : Superoxide Dismutase Isoforms in the Vessel Wall
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 24, No. 8 ( 2004-08), p. 1367-1373
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 8 ( 2004-08), p. 1367-1373
    Abstract: Recent studies have begun to define the role of specific isoforms of superoxide dismutase (SOD) in vascular biology. This review focuses on the role of SODs in vessels in health and disease. This area is important because reactive oxygen species are thought to play a major role in vascular pathophysiology.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000133604.20182.cf
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1494427-3
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  • 10
    Online Resource
    Online Resource
    IL-6 Deficiency Protects Against Angiotensin II–Induced Endothelial Dysfunction and Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 27, No. 12 ( 2007-12), p. 2576-2581
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 27, No. 12 ( 2007-12), p. 2576-2581
    Abstract: The role of IL-6 in endothelial dysfunction and oxidative stress produced by angiotensin II was investigated. IL-6 deficiency was associated with reductions in angiotensin II–induced endothelial dysfunction, vascular hypertrophy, and superoxide. Thus, IL-6 produced locally, within the vessel wall, contributes substantially to the vascular dysfunction produced by angiotensin II.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.107.153080
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1494427-3
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