scholarly journals Temporal effects of 17β-estradiol on caveolin-1 mRNA and protein in bovine aortic endothelial cells

2001 ◽  
Vol 281 (3) ◽  
pp. H1327-H1333 ◽  
Author(s):  
Muthuvel Jayachandran ◽  
Toshio Hayashi ◽  
Daigo Sumi ◽  
Akihisa Iguchi ◽  
Virginia M. Miller
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Estrogen Receptor ◽  
Aortic Endothelial Cells ◽  
Caveolin 1 ◽  
Bovine Aortic Endothelial Cells ◽  
17Β Estradiol ◽  
Nitrite Nitrate ◽  
Enos Protein ◽  
Aortic Endothelial

Endothelial nitric oxide synthase (eNOS) is regulated both by caveolin-1 and 17β-estradiol (E2). Temporal relationships between effects of estrogen on caveolin-1 and nitric oxide (NO) are not known. Therefore, this study was designed to determine whether estrogen regulates caveolin-1 and, if so, whether such regulation corresponds to changes in nitrite/nitrate (NOx) production. Bovine aortic endothelial cells (BAECs) were cultured in the absence and presence of 17β-estradiol or 17α-estradiol (10−8 and 10−10 M) for 12, 24, and 48 h. eNOS protein expression and NOx production increased significantly after 24 h but not after 12-h treatment with 17β- and not 17α-estradiol. Both mRNA and protein for caveolin-1 were increased significantly only after 48-h treatment with E2, but eNOS protein and NOx production were decreased compared with cells treated for 24 h. These increases in caveolin-1 were inhibited by the estrogen receptor antagonist ICI-182,780 (10−6 M). Results of this study suggest that E2 stimulates caveolin-1 transcription and translation through estrogen receptor-mediated mechanisms. The results further suggest that estrogen may indirectly regulate NOx through caveolin-1 expression, which inhibits eNOS catalytic activity.

Arginine or citrulline associated with a statin stimulates nitric oxide production in bovine aortic endothelial cells

2011 ◽  
Vol 670 (2-3) ◽  
pp. 566-570 ◽  
Author(s):  
Marie-Clotilde Berthe ◽  
Mélisande Bernard ◽  
Carole Rasmusen ◽  
Sylviane Darquy ◽  
Luc Cynober ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Production ◽  
Aortic Endothelial Cells ◽  
Oxide Production ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

Large Negative Stress Phase Angle (SPA) Attenuates Nitric Oxide Production in Bovine Aortic Endothelial Cells

2006 ◽  
Vol 128 (3) ◽  
pp. 329-334 ◽  
Author(s):  
Michael B. Dancu ◽  
John M. Tarbell
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Phase Angle ◽  
Aortic Endothelial Cells ◽  
Temporal Phase ◽  
Bovine Aortic Endothelial Cells ◽  
Stress Phase Angle ◽  
Aortic Endothelial

Hemodynamics plays an important role in cardiovascular physiology and pathology. Pulsatile flow (Q), pressure (P), and diameter (D) waveforms exert wall shear stress (WSS), normal stress, and circumferential strain (CS) on blood vessels. Most in vitro studies to date have focused on either WSS or CS but not their interaction. Recently, we have shown that concomitant WSS and CS affect EC biochemical response modulated by the temporal phase angle between WSS and CS (stress phase angle, SPA). Large negative SPA has been shown to occur in regions of the circulation where atherosclerosis and intimal hyperplasia are prevalent. Here, we report that nitric oxide (NO) biochemical secretion was significantly decreased in response to a large negative SPA of −180 deg with respect to an SPA of 0° in bovine aortic endothelial cells (BAEC) at 5 h. A new hemodynamic simulator for the study of the physiologic SPA was used to provide the hemodynamic conditions of pro-atherogenic (SPA=−180 deg) and normopathic (SPA=0 deg) states. The role of complex hemodynamics in vascular remodeling, homeostasis, and pathogenesis can be advanced by further assessment of the hypothesis that a large negative SPA is pro-atherogenic.

Volatile Anesthetics Affect Calcium Mobilization in Bovine Endothelial Cells

1996 ◽  
Vol 85 (5) ◽  
pp. 1147-1156 ◽  
Author(s):  
Thomas N. Pajewski ◽  
Ning Miao ◽  
Carl III Lynch ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Adenosine Triphosphate ◽  
Volatile Anesthetic ◽  
Volatile Anesthetics ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Inhalational Anesthetics ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

Background The site where volatile anesthetics inhibit endothelium-dependent, nitric oxide-mediated vasodilation is unclear. To determine whether anesthetics could limit endothelium-dependent nitric oxide production by inhibiting receptor-mediated increases in cytosolic Ca2+, experiments were performed to see if the inhalational anesthetics halothane, isoflurane, and enflurane affect intracellular Ca2+ ([Ca2+]i) transients induced by the agonists bradykinin and adenosine triphosphate in cultured bovine aortic endothelial cells. Methods Bovine aortic endothelial cells, which had been loaded with the fluorescent Ca2+ indicator Fura-2, were added to medium preequilibrated with volatile anesthetic (1.25% and 2.5% for isoflurane, 1.755 and 3.5% for enflurane, and 0.75% and 1.5% for halothane). In Ca(2+)-containing medium, intracellular Ca2+ transients were elicited in response to bradykinin (10 nM and 1 microM) or adenosine triphosphate (1 microM and 100 microM). Results Both bradykinin and adenosine triphosphate triggered a rapid rise to peak [Ca2+]i followed by a gradual decline to a plateau above the resting level. Although basal [Ca2+]i was unaltered by the anesthetics, both halothane and enflurane, in a dose-dependent manner, depressed the peak and plateau of the [Ca2+]i transient elicited by 10 nM bradykinin, whereas isoflurane had no effect. When [Ca2+]i transients were elicited by 1 microM bradykinin, halothane (1% and 5%) did not alter peak and plateau levels. Halothane and enflurane also decreased [Ca2+]i transients evoked by 1 microM and 100 microM adenosine triphosphate, whereas isoflurane also had no effect in this setting. Conclusions Halothane and enflurane, but not isoflurane, inhibit bradykinin- and adenosine triphosphate-stimulated Ca2+ transients in endothelial cells. Limitations of Ca2+ availability to activate constitutive endothelial nitric oxide synthase could allow for part, but not all, of the inhibition of endothelium-dependent nitric oxide-mediated vasodilation by inhalational anesthetics.

Release of NO and EDRF from cultured bovine aortic endothelial cells

1989 ◽  
Vol 256 (4) ◽  
pp. H1030-H1037 ◽  
Author(s):  
P. R. Myers ◽  
R. Guerra ◽  
D. G. Harrison
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Sodium Iodide ◽  
Aortic Endothelial Cells ◽  
Prostaglandin F2 Alpha ◽  
Bovine Aortic Endothelial Cells ◽  
Reducing Environment ◽  
Vasorelaxant Activity ◽  
Endothelium Derived Relaxing Factor ◽  
Aortic Endothelial

The endothelium-derived relaxing factor (EDRF) has recently been reported to be nitric oxide. This study was performed to determine whether the vasorelaxant activity of EDRF could be accounted for by nitric oxide released from cultured endothelial cells. Nitric oxide released from cultured bovine aortic endothelial cells was monitored using a chemiluminescence technique with and without reflux processing of the effluent with a strong reducing environment (1% sodium iodide in glacial acetic acid). In the presence of indomethacin, basally released EDRF was sufficient to relax a bioassay detector vessel (preconstricted with prostaglandin F2 alpha) by 41 +/- 8%. Bradykinin (0.01 microM) and A23187 (10 microM) produced relaxation of the bioassay detector vessel equal to 74 +/- 7 and 69 +/- 13%, respectively. In both the absence and the presence of reflux preprocessing of the cell effluent in a reducing environment, the amount of nitric oxide detected by chemiluminescence was 7-10-fold less than that required to account for the detector vessel relaxation (determined from responses of the detector vessel to standard infusions of authentic nitric oxide). These experiments contradict the view that nitric oxide is the sole or principal EDRF. It is likely that either other nonprostanoid vasodilator substances are released in addition to nitric oxide or that EDRF is a nitric oxide containing or forming compound that is substantially more potent than authentic nitric oxide.

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