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W Kossenjans

Publications and source records attributed to W Kossenjans.

14 recordsLinked to original sources
PubMed2000

Role of peroxynitrite in altered fetal-placental vascular reactivity in diabetes or preeclampsia.

Oxidative stress may increase production of superoxide and nitric oxide, leading to formation of prooxidant peroxynitrite to cause vascular dysfunction. Having found nitrotyrosine residues, a marker of peroxynitrite action, in placental vessels of preeclamptic and diabetic pregnancies, we determined whether vasoreactivity is altered in these placentas and treatment with peroxynitrite produces vascular dysfunction. The responses of diabetic, preeclamptic, and normal placentas to increasing concentrations of the vasoconstrictors U-46619 (10(-9)-10(-7) M) and ANG II (10(-9)-10(-7) M) and the vasodilators glyceryl trinitrate (10(-9)-10(-7) M) and prostacyclin (PGI(2); 10(-8)-10(-6) M) were compared as were responses to these agents in normal placentas before and after treatment with 3.16 x 10(-4) M peroxynitrite for 30 min. Responses to both vasoconstrictors and vasodilators were significantly attenuated in diabetic and preeclamptic placentas compared with controls. Similarly, responses to U-46619, nitroglycerin, and PGI(2), but not ANG II, were significantly attenuated following peroxynitrite treatment. The presence of nitrotyrosine residues confirmed peroxynitrite interaction with placental vessels. Overall, our data suggest that peroxynitrite formation is capable of attenuating vascular responses in the human placenta.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Comparative localization of endothelial and inducible nitric oxide synthase isoforms in haemochorial and epitheliochorial placentae.

The presence and immunolocalization of type II (inducible or macrophage) and type III (endothelial) nitric oxide synthase (NOS) isoforms were compared in the term placentae of humans, rhesus monkeys, baboons, guinea-pigs, rats and sheep using isoform specific antibodies. In the human placenta, intense immunohistochemical staining for type III NOS was seen in syncytiotrophoblast with weaker staining in vascular endothelial cells. Only vascular endothelial cells showed positive III NOS staining in rhesus monkey, baboon, guinea-pig, rat and sheep placentae. No positive type III NOS immunostaining was seen in trophoblast from any non-human placentae. Western blotting revealed a 135-kDa type III NOS species in placental homogenates, semi-purified by ADP-sepharose affinity chromatography, from all the species tested confirming antibody specificity. Type II NOS immunostaining was localized to certain villous stromal cells which also stained for CD14 (a monocyte/macrophage marker) in the placenta of humans, rhesus monkeys, baboons and sheep. No specific immunohistochemical staining for type II NOS or CD14 was noted in the two rodent species, guinea-pig and rat. On Western blots, a 130-kDa type II NOS species was identified in semi-purified placental homogenates of every species except guinea-pig, although weak bands were seen for rhesus monkey and baboon. The failure of the antibodies to show type II NOS in the rat placenta by immunohistochemistry may be due to a difference in antigen conformation from Western blots. As only human placental syncytiotrophoblast expresses type III NOS, the putative functions ascribed to this isoform in syncytiotrophoblast, i.e., to prevent platelet and leucocyte aggregation in the intervillous space and adhesion to the trophoblast surface or to mediate peptide hormone release from trophoblast, may be unique to humans. Alternatively, syncytiotrophoblast-derived NO may fulfill some other unknown function. The similar pattern of expression of type II NOS in those species with villous fetomaternal interdigitation and multivillous fetomaternal blood flow interrelations may represent a more universal role in surveillance and/or protection against maternal insults or pathogens by immunologic activation and subsequent synthesis of nitric oxide which exerts a cytostatic/cytotoxic response.

Animals↗
PubMed1997

Inducible (type II) nitric oxide synthase in human placental villous tissue of normotensive, pre-eclamptic and intrauterine growth-restricted pregnancies.

We have utilized two distinct monospecific antibodies against the type II (macrophage or inducible) nitric oxide synthase (NOS) isoform to localize the distribution of the enzyme within the human placenta in tissues from normotensive pregnancies and those complicated by pre-eclampsia and/or intrauterine growth restriction. Both antibodies immunolocalize to cells in the villous stroma on frozen sections of villous tissue. Colocalization studies with anti-CD14 or anti-CD45 antibodies that recognize cells of leucocyte or monocyte/macrophage lineage indicate that Hofbauer cells are expressing type II NOS. This is in contrast to expression of type III (endothelial) NOS which is seen in syncytiotrophoblast and in villous vascular endothelium. In some, but not all, normotensive and pathologic placental tissue, some type II NOS immunostaining could be seen in syncytiotrophoblast and vascular endothelium; however, no differences could be discerned between groups of tissues. Expression of type II NOS by Hofbauer cells may indicate they are involved in surveillance against maternal immune insult or maternal pathogens whereby they secrete nitric oxide to exert a cytostatic/cytotoxic effect.

Female↗
PubMed1997

Differential localization of superoxide dismutase isoforms in placental villous tissue of normotensive, pre-eclamptic, and intrauterine growth-restricted pregnancies.

Several isoforms of superoxide dismutase (SOD), including copper/zinc (cytosolic) and manganese (mitochondrial), exist. In the human placenta, SOD may prevent excessive superoxide accumulation and any potential deleterious oxidative effects. In pre-eclampsia, increased levels of lipid peroxide and decreased SOD activity have been described in the placenta. Oxidative stress such as occurs in pre-eclampsia can alter expression of SOD isoforms. The objective of this study was to localize the copper/zinc and manganese SOD isoforms in the placenta using immunohistochemistry and to compare localization and intensity of immunostaining in tissues from normotensive pregnancies with those from pregnancies complicated by pre-eclampsia and/or intrauterine growth restriction (IUGR). Western blotting with specific antibodies recognized a 17-kD copper/zinc and a 23-kD manganese SOD subunit in placental homogenates. Intense immunostaining for the manganese SOD isoform was seen in villous vascular endothelium, but only faint staining was found in the syncytiotrophoblast or villous stroma. In serial sections, intense immunostaining for copper/zinc SOD was seen in certain cells of the villous stroma but only faint immunostaining in syncytiotrophoblast and vascular endothelium. No apparent differences in localization or intensity of immunostaining for either isoform were seen between tissues of normotensive or pre-eclamptic pregnancies, with or without IUGR. The different cellular localizations of the SOD isoforms suggest that they fulfill different functional roles within the placenta.

Blotting, Western↗
PubMed1996

Menadione-induced oxidative stress in bovine heart microvascular endothelial cells.

OBJECTIVE: Oxidative stress from increased production of reactive oxygen species or decreased efficiency of inhibitory and scavenger systems may contribute to vascular injury. In this study, we developed an in vitro model of vascular injury by menadione-induced oxidative stress in bovine heart microvascular endothelial cells. METHODS: Oxidative stress was induced by exposure to menadione. Superoxide, hydrogen peroxide and hydroxyl radical formation was measured by superoxide dismutase-inhibitable cytochrome c reduction, the dichlorofluorescin technique and the salicylate method, respectively. Electron paramagnetic-spin resonance spectroscopy employing 5-5'-dimethyl-l-pyrroline-N-oxide for superoxide trapping was used. Endothelial cell cytotoxicity was assessed by lactate dehydrogenase release. RESULTS: Superoxide and hydroxyl radical were produced in a time- and concentration-dependent fashion. Fluorescence in the presence of dichlorofluorescin confirmed hydrogen peroxide formation. Endothelial cell cytotoxicity became evident after 5 h of menadione treatment at concentrations of 100 microM. 3-Aminobenzamide, a poly(ADP-ribose)polymerase inhibitor, and dimethylthiourea, a hydrogen peroxide and hydroxyl radical scavenger, decreased menadione cytotoxicity, whereas deferoxamine, an inhibitor of hydroxyl radical formation, did not. CONCLUSIONS: The results suggest that menadione toxicity is mediated by poly(ADP-ribose)polymerase activation via hydrogen peroxide formation and that menadione-treated bovine heart microvessel endothelial cells provide a suitable in vitro model to study oxidative stress in endothelial cells.

Animals↗
PubMed1995

The action of two natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide) in the human placental vasculature.

OBJECTIVE: Our purpose was to compare the actions of atrial natriuretic peptide and brain natriuretic peptide in the human placental vasculature. STUDY DESIGN: Isolated placental cotyledons were dually perfused with fetal perfusion pressure used as an index of vascular response. The effect of angiotensin II (10(-10) to 10(-6) mol/L bolus injection) was established in the absence or presence of atrial natriuretic peptide (10(-8) mol/L) or brain natriuretic peptide (10(-8) mol/L final concentration). The role of nitric oxide as a mediator of natriuretic peptide action was investigated by perfusion of n-nitro-L-arginine (10(-3) mol/L), an inhibitor of nitric oxide synthase. Attenuation of the action of atrial natriuretic peptide by placental peptidases was studied by perfusion with the peptidase inhibitor benzamidine (2 x 10(-2) mol/L). Statistical significance was determined by analysis of variance and paired t test. RESULTS: Significant attenuation of vasoconstrictor responses to angiotensin II occurred within both atrial natriuretic peptide and brain natriuretic peptide; however, brain natriuretic peptide was more effective. n-Nitro-L-arginine did not affect the attenuation of angiotensin II-induced vasoconstriction by atrial or brain natriuretic peptides. In the presence of benzamidine atrial natriuretic peptide exerted a significantly greater vasodilator effect. CONCLUSION: Brain natriuretic peptide is a more potent vasodilator of the placental vasculature than is atrial natriuretic peptide. The low efficacy of atrial natriuretic peptide may be related to placental peptidases. Nitric oxide does not mediate the action of atrial natriuretic peptide or brain natriuretic peptide.

Angiotensin II↗
PubMed1995

The interaction of nitric oxide and superoxide in the human fetal-placental vasculature.

OBJECTIVE: Our purpose was to study the interaction of nitric oxide and superoxide anion on the vasculature of the isolated perfused human placental cotyledon. STUDY DESIGN: Isolated placental cotyledons were preconstricted with the thromboxane mimetic U46619, and fetal perfusion pressure was used as an index of response. The interaction of nitric oxide and O2- was studied by three protocols: (1) with endogenous nitric oxide, (2) with addition of exogenous nitric oxide, and (3) with inhibition of nitric oxide synthesis by the nitric oxide synthase inhibitor N-nitro-L-arginine. O2- was generated by infusion of purine-xanthine oxidase. Statistical significance of response to treatment was determined by paired t test. RESULTS: Infusion of xanthine oxidase with purine in the presence of endogenous nitric oxide resulted in vasodilation (p < 0.05). Vasodilation was more pronounced in the presence of exogenous nitric oxide (p < 0.008). Coinfusion of xanthine oxidase with purine in the presence of N-nitro-L-arginine to inhibit nitric oxide synthesis resulted in vasoconstriction. CONCLUSION: We conclude that, rather than superoxide inactivating nitric oxide, interaction of the two radicals generates in the placental vasculature a vasodilator, which may be peroxynitrite.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Interaction of angiotensin II and brain natriuretic peptide in the placentas of normal and diabetic women.

OBJECTIVE: To evaluate the effects of angiotensin II and brain natriuretic peptide on the placental vasculature of diabetic women. METHODS: Term placentas from five diabetic women and five nondiabetic controls were collected. Isolated placental cotyledons were perfused dually with fetal perfusion pressure as an index of vascular response. The effect of angiotensin II (10(-10)-10(-5) mol/L bolus injection) was established in the fetal-placental vasculature of all placentas in the absence or presence of brain natriuretic peptide (10(-8) mol/L final concentration). Data were analyzed using repeated measures analysis of variance and paired t test where appropriate. RESULTS: A significant vasoconstrictor response to angiotensin II was achieved in placentas of both diabetic and nondiabetic women (P < .001); however, the angiotensin II-induced increase in perfusion pressure was significantly greater in the diabetic group (P < .01). Significant attenuation of vasoconstrictor response to angiotensin occurred in the presence of brain natriuretic peptide in placentas of both nondiabetic (P < .0025) and diabetic (P < .025) women, but the effect was more prominent in the diabetic group. CONCLUSION: The in vitro placental vasculature of diabetic women is more sensitive to angiotensin II than is the in vitro placental vasculature of nondiabetic women. The attenuation exerted by brain natriuretic peptide on angiotensin II-induced vasoconstriction is more prominent in placentas from diabetic women compared to those from nondiabetic women.

Adult↗
PubMed1991

Evidence of zein-bound indoleacetic Acid using gas chromatography-selected ion monitoring-mass spectrometry analysis and immunogold labeling.

Commercial zein was base-hydrolyzed and purified extracts were subjected to gas chromatography-selected ion monitoring-mass spectrometry analysis. Indoleacetic acid (IAA) was shown to be released from this storage protein of corn (Zea mays). Isotope dilution using [(13)C(6)]IAA as an internal standard revealed a conservative ratio of 1 mole IAA to 175 moles zein. Immunoelectron micrographs of isolated protein bodies also showed IAA or an IAA-like molecule associated with zein and deposited within these organelles.

Journal Article↗
PubMed1988

Localization of sodium-potassium adenosine triphosphatase in sheep myocardium by immunoelectron microscopy.

Immunohistochemical localization of sodium and potassium dependent adenosine triphosphatase (Na,K-ATPase) employing polyclonal antibodies was carried out on sheep myocardium. The tissue was fixed with glutaraldehyde or a paraformaldehyde/lysine/periodate combination fixative and embedded in different embedding media. Ultrathin sections were labeled with rabbit anti-sheep Na,K-ATPase antiserum followed by sheep anti-rabbit immunoglobulin complexed with colloidal gold. Glycol methacrylate embedded tissue provided good structural preservation and showed specific immunohistochemical labeling. Analysis of the gold particle distribution showed a significantly higher number of Na,K-ATPase immunoreactive sites associated with cell membrane and T-tubules.

Animals↗
PubMed1988

Cytochrome C, a potent oxygen free radical scavenger against the calcium paradox injury in the myocardium.

The calcium paradox was induced by perfusion of hearts with a calcium-free medium for 10 mins followed by calcium-containing medium for 20 mins (group A). During calcium depletion, myocytes were preserved but vascular endothelial cells underwent prominent morphological changes and their plasma membranes were disrupted and transformed to myelin-like whorls. Calcium repletion induced severe myocyte necrosis, massive release of creatine phosphokinase (CPK) and calcium accumulation. The effect of ferricytochrome C on the calcium paradox injury was investigated in groups of hearts; ferricytochrome C (75 microM) was given either during calcium repletion only (group B), during calcium depletion only (group C), or both during calcium depletion and repletion (group D). There was no protection by cytochrome C in group B with no reduction in release of CPK, calcium accumulation or cell damage. However, cytochrome C was very protective when given during calcium depletion (groups C and D). CPK was significantly reduced in groups C and D compared to group A (P less than 0.03) and less calcium accumulation was observed in groups C and D (6.0 +/- 0.8, 12.5 +/- 1.25 mumol) compared to group A (P less than 0.03). Moreover, a significant number of cells was preserved in group C (84%) and group D (80%), compared to group A (2%). This was associated with prevention of vascular damage caused by calcium depletion. The data provide strong evidence that cytochrome C is a potent protective agent against the calcium paradox injury that may be caused by oxygen-derived radicals.

Animals↗
PubMedDate not supplied

Oxidative stress causes vascular dysfunction in the placenta.

Increased production of superoxide and nitric oxide may produce oxidative stress in the placenta by formation of the prooxidant peroxynitrite, which itself causes vascular dysfunction. Nitrotyrosine residues, which are a marker of peroxynitrite formation and action, are found in placental vessels of preeclamptic and diabetic pregnancies, indicating oxidative stress. Treatment of the placental vasculature with authentic peroxynitrite in vitro attenuates responses both to vasoconstrictors such as the thromboxane mimetic U46619 and to vasodilators, including glyceryl trinitrate and prostacyclin, indicating it has caused vascular dysfunction. Further, the responses of the fetal-placental vasculature of diabetic and preeclamptic placentae to these same vasoconstrictor and vasodilator agents are significantly attenuated when compared to responses in normal control placentae. Together these data suggest there may be a cause and effect relationship between formation and action of peroxynitrite and vascular dysfunction in the placenta of both preeclamptic and diabetic pregnancies. The presence of such attenuated vascular responses indicates that perhaps the placenta may not be able to adequately respond to demands for altered blood flow in situations where this is necessary in preeclamptic or diabetic pregnancies, thus leading to further fetal compromise.

Blood Vessels↗
PubMedDate not supplied

Selective vasodilator effects of atrial natriuretic peptide in the human placental vasculature.

OBJECTIVE: To determine whether atrial natriuretic peptide (ANP) attenuates the vasoconstrictor effects of angiotensin II (AII), a thromboxane mimetic (U46619), and endothelin-1 in the human fetal-placental vasculature and to determine whether nitric oxide (NO) has a role in the vasodilator activity of ANP. METHODS: Isolated placental cotyledons were dually perfused, with fetal perfusion pressure used as an index of vascular response. The effects of AII (10(-10)-10(-6) mol/L bolus injection), endothelin-1 (10(-7) mol/L bolus), and U46619 (10(-9)-10(-6) mol/L bolus or 10(-8) mol/L infusion) were established in the absence or presence of ANP (10(-8) mol/L). The role of NO as a mediator of ANP action was investigated by perfusion with n-nitro-L-arginine (NNLA, 10(-3) mol/L), an inhibitor of NO synthase. Statistical significance was determined by analysis of variance. RESULTS: Atrial natriuretic peptide caused significant attenuation of vasoconstrictor responses to AII, but weak attenuation of endothelin-1 and no attenuation of U46619. Use of NNLA did not affect the attenuation of AII-induced vasoconstriction by ANP. CONCLUSIONS: Atrial natriuretic peptide is a vasodilator of the fetal-placental vasculature constricted with AII and endothelin-1, but not with U46619. Nitric oxide does not mediate the action of ANP.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗