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Article ; Online: H2O2 is the transferrable factor mediating flow-induced dilation in human coronary arterioles.

Liu, Yanping / Bubolz, Aaron H / Mendoza, Suelhem / Zhang, David X / Gutterman, David D

2011 Volume 108, Issue 5, Page(s) 566–573

Abstract: Rationale: Endothelial derived hydrogen peroxide (H(2)O(2)) is a necessary component ... of the pathway regulating flow-mediated dilation (FMD) in human coronary arterioles (HCAs). However, H(2)O(2) has ... in response to shear stress.: Objective: We examined the hypothesis that H(2)O(2) serves as the EDHF ...

Abstract	Rationale: Endothelial derived hydrogen peroxide (H(2)O(2)) is a necessary component of the pathway regulating flow-mediated dilation (FMD) in human coronary arterioles (HCAs). However, H(2)O(2) has never been shown to be the endothelium-dependent transferrable hyperpolarization factor (EDHF) in response to shear stress. Objective: We examined the hypothesis that H(2)O(2) serves as the EDHF in HCAs to shear stress. Methods and results: Two HCAs were cannulated in series (a donor intact vessel upstream and endothelium-denuded detector vessel downstream). Diameter changes to flow were examined in the absence and presence of polyethylene glycol catalase (PEG-CAT). The open state probability of large conductance Ca(2+)-activated K(+) (BK(Ca)) channels in smooth muscle cells downstream from the perfusate from an endothelium-intact arteriole was examined by patch clamping. In some experiments, a cyanogen bromide-activated resin column bound with CAT was used to remove H(2)O(2) from the donor vessel. When flow proceeds from donor to detector, both vessels dilate (donor:68±7%; detector: 45±11%). With flow in the opposite direction, only the donor vessel dilates. PEG-CAT contacting only the detector vessel blocked FMD in that vessel (6±4%) but not in donor vessel (61±13%). Paxilline inhibited dilation of endothelium-denuded HCAs to H(2)O(2). Effluent from donor vessels elicited K(+) channel opening in an iberiotoxin- or PEG-CAT-sensitive fashion in cell-attached patches but had little effect on channel opening on inside-out patches. Vasodilation of detector vessels was diminished when exposed to effluent from CAT-column. Conclusions: Flow induced endothelial production of H(2)O(2), which acts as the transferrable EDHF activating BK(Ca) channels on the smooth muscle cells.
MeSH term(s)	Arterioles/drug effects ; Arterioles/physiology ; Biological Factors/metabolism ; Catalase/metabolism ; Coronary Vessels/drug effects ; Coronary Vessels/physiology ; Endothelium, Vascular/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Hydrogen Peroxide/pharmacology ; Indoles/pharmacology ; Large-Conductance Calcium-Activated Potassium Channels/metabolism ; Muscle, Smooth, Vascular/metabolism ; Patch-Clamp Techniques ; Polyethylene Glycols/metabolism ; Potassium Channel Blockers/pharmacology ; Regional Blood Flow/physiology ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Biological Factors ; Indoles ; Large-Conductance Calcium-Activated Potassium Channels ; Potassium Channel Blockers ; catalase-polyethylene glycol ; endothelium-dependent hyperpolarization factor ; paxilline (3T9U9Z96L7) ; Polyethylene Glycols (3WJQ0SDW1A) ; Hydrogen Peroxide (BBX060AN9V) ; Catalase (EC 1.11.1.6)
Language	English
Publishing date	2011-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.110.237636
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Article ; Online: Bradykinin-induced dilation of human coronary arterioles requires NADPH oxidase-derived reactive oxygen species.

Larsen, Brandon T / Bubolz, Aaron H / Mendoza, Suelhem A / Pritchard, Kirkwood A / Gutterman, David D

Arteriosclerosis, thrombosis, and vascular biology

2009 Volume 29, Issue 5, Page(s) 739–745

Abstract: Objective: Hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor in human coronary arterioles (HCAs). H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the ... ...

Abstract	Objective: Hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor in human coronary arterioles (HCAs). H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown. Methods and results: NADPH oxidase expression was determined by immunohistochemistry. Superoxide and H2O2 production was assayed in HCAs and human coronary artery endothelial cells (HCAECs) using dihydroethidium and dichlorodihydrofluorescein histofluorescence, respectively. Superoxide was quantified by HPLC separation of dihydroethidium products. Diameter changes of HCAs were measured by videomicroscopy. NADPH oxidase subunits Nox1, Nox2, Nox4, p22, p47, and p67 were each expressed in HCA endothelium. In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone. HPLC analysis confirmed that BK specifically induced superoxide production. Gp91ds-tat reduced vasodilation to BK but not to papaverine. 14,15-EEZE (an EET antagonist) further reduced the residual dilation to BK in the presence of gp91ds-tat, but had no effect in the presence of gp91scram-tat, suggesting that NADPH oxidase-derived ROS modulate EET bioavailability. Conclusion: We conclude that endothelial NADPH oxidase is a functionally relevant source of H2O2 that mediates agonist-induced dilation in the human heart.
MeSH term(s)	Aged ; Aged, 80 and over ; Bradykinin/physiology ; Coronary Vessels/metabolism ; Female ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Middle Aged ; NADPH Oxidases/metabolism ; Vasodilation/physiology
Chemical Substances	Hydrogen Peroxide (BBX060AN9V) ; NADPH Oxidases (EC 1.6.3.-) ; Bradykinin (S8TIM42R2W)
Language	English
Publishing date	2009-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.108.169367
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Article: Enhanced oxidative stress impairs cAMP-mediated dilation by reducing Kv channel function in small coronary arteries of diabetic rats.

Bubolz, Aaron H / Li, Hongwei / Wu, Qingping / Liu, Yanping

American journal of physiology. Heart and circulatory physiology

2005 Volume 289, Issue 5, Page(s) H1873–80

Abstract: We have shown that short-term exposure of rat small coronary arteries (RSCAs) to high glucose enhances superoxide (O2-*) formation and impairs cAMP-mediated dilation by reducing voltage-gated K+ (Kv) channel function. However, it is not clear whether the ...

Abstract	We have shown that short-term exposure of rat small coronary arteries (RSCAs) to high glucose enhances superoxide (O2-) formation and impairs cAMP-mediated dilation by reducing voltage-gated K+ (Kv) channel function. However, it is not clear whether the impairment also occurs in diabetes mellitus (DM), where alternate mechanisms could mask or aggravate vasodilator dysfunction. RSCAs were isolated from control and streptozotocin-induced diabetic rats. Reduced constriction to 4-aminopyridine (4-AP) was observed in RSCAs from DM rats, indicating Kv channel impairment. Forskolin increased 4-AP-inhibitable K+ channel open-state probability and whole cell K+ current density in coronary myocytes from non-DM rats but had little effect on K+ current density in cells from DM rats. Diminished dilation to 8-bromo-cAMP, forskolin, or isoproterenol was observed in DM RSCAs. The attenuated dilation to forskolin or isoproterenol in DM RSCAs was partially restored by application of the superoxide dismutase mimetic manganese[III] tetrakis (4-benzoic acid) porphyrin. Histofluorescence studies using hydroethidine revealed a blockage of O2- generation by the NADPH oxidase inhibitor apocynin in DM RSCAs. Sepiapterin, a precursor of tetrahydrobiopterin, had little effect on hyperglycemia-induced O2-* formation. Consistent with the findings from the concurrent fluorescence study, apocynin also partially restored the reduced dilator response to forskolin in DM RSCAs. Forskolin-induced cAMP production was unaltered in DM. We conclude that in diabetes, enhanced O2-* formation by activation of NADPH oxidase impairs cAMP-medicated dilation in RSCAs by inhibiting Kv channel activity.
MeSH term(s)	4-Aminopyridine/pharmacology ; Animals ; Antioxidants/pharmacology ; Blood Glucose/metabolism ; Body Weight/physiology ; Colforsin/pharmacology ; Coronary Vessels/drug effects ; Coronary Vessels/physiopathology ; Cyclic AMP/biosynthesis ; Cyclic AMP/physiology ; Diabetes Mellitus, Experimental/physiopathology ; Male ; Microscopy, Video ; Muscle Contraction/drug effects ; NADPH Oxidases/antagonists & inhibitors ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Patch-Clamp Techniques ; Potassium Channel Blockers/pharmacology ; Potassium Channels/drug effects ; Potassium Channels/physiology ; Rats ; Rats, Sprague-Dawley ; Spectrometry, Fluorescence ; Superoxides/metabolism ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Antioxidants ; Blood Glucose ; Potassium Channel Blockers ; Potassium Channels ; Superoxides (11062-77-4) ; Colforsin (1F7A44V6OU) ; 4-Aminopyridine (BH3B64OKL9) ; Cyclic AMP (E0399OZS9N) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2005-06-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00357.2005
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Article: Endothelial cytoskeletal elements are critical for flow-mediated dilation in human coronary arterioles.

Liu, Yanping / Li, Hongwei / Bubolz, Aaron H / Zhang, David X / Gutterman, David D

Medical & biological engineering & computing

2008 Volume 46, Issue 5, Page(s) 469–478

Abstract: Mitochondrial H2O2 contributes to flow-mediated dilation (FMD) in human coronary arterioles (HCA). We examined the hypothesis that the endothelial cytoskeleton plays a critical role in transducing endothelial wall shear stress into a stimulus for ... ...

Abstract	Mitochondrial H2O2 contributes to flow-mediated dilation (FMD) in human coronary arterioles (HCA). We examined the hypothesis that the endothelial cytoskeleton plays a critical role in transducing endothelial wall shear stress into a stimulus for releasing mitochondrial ROS. Phallacidin together with alpha-, beta-tubulin antibodies and Mito-Tracker Red showed the proximity of F-actin, microtubules and mitochondria in endothelial cells. Cytochalasin D (CytoD) and nocodazole (Noc) disrupted endothelial F-actin and microtubules in HCA, respectively, concurrent with a reduction in the generation of cytosolic and H2O2 (hydroethidine and dichlorodihydrofluorescein fluorescence) and mitochondrial superoxide (mitoSox) during flow (control: 3.5 +/- 1.6, Cyto D: 0.51 +/- 0.2, Noc: 0.81 +/- 0.6). FMD, but not the dilation to bradykinin or papaverine, was reduced by Cyto D (26 +/- 10% vs. 56 +/- 3%) or Noc (26 +/- 11% vs. 58 +/- 7%). These results suggest that cytoskeletal elements are a critical component of the signaling mechanism linking endothelial shear stress and mitochondrial release of ROS in the human coronary microcirculation.
MeSH term(s)	Aged ; Arterioles/ultrastructure ; Cells, Cultured ; Coronary Circulation ; Coronary Vessels ; Cytoskeletal Proteins/metabolism ; Cytoskeleton/metabolism ; Endothelium, Vascular/ultrastructure ; Female ; Humans ; Male ; Vasodilation/physiology
Chemical Substances	Cytoskeletal Proteins
Language	English
Publishing date	2008-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	282327-5
ISSN	1741-0444 ; 0140-0118 ; 0025-696X
ISSN (online)	1741-0444
ISSN	0140-0118 ; 0025-696X
DOI	10.1007/s11517-008-0331-1
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Article ; Online: Activation of endothelial TRPV4 channels mediates flow-induced dilation in human coronary arterioles: role of Ca2+ entry and mitochondrial ROS signaling.

Bubolz, Aaron H / Mendoza, Suelhem A / Zheng, Xiaodong / Zinkevich, Natalya S / Li, Rongshan / Gutterman, David D / Zhang, David X

American journal of physiology. Heart and circulatory physiology

2011 Volume 302, Issue 3, Page(s) H634–42

Abstract: ... dilation is mediated by a unique mechanism involving the release of H(2)O(2) from the mitochondria ... of endothelial cells (ECs). How flow activates ECs to elicit the mitochondrial release of H(2)O(2) remains unclear ... by catalase, a H(2)O(2)-metabolizing enzyme. Fluorescence ROS assays showed that 4α-PDD increased ...

Abstract	In human coronary arterioles (HCAs) from patients with coronary artery disease, flow-induced dilation is mediated by a unique mechanism involving the release of H(2)O(2) from the mitochondria of endothelial cells (ECs). How flow activates ECs to elicit the mitochondrial release of H(2)O(2) remains unclear. Here, we examined the role of the transient receptor potential vanilloid type 4 (TRPV4) channel, a mechanosensitive Ca(2+)-permeable cation channel, in mediating ROS formation and flow-induced dilation in HCAs. Using RT-PCR, Western blot analysis, and immunohistochemical analysis, we detected the mRNA and protein expression of TRPV4 channels in ECs of HCAs and cultured human coronary artery ECs (HCAECs). In HCAECs, 4α-phorbol-12,13-didecanoate (4α-PDD), a selective TRPV4 agonist, markedly increased (via Ca(2+) influx) intracellular Ca(2+) concentration. In isolated HCAs, activation of TRPV4 channels by 4α-PDD resulted in a potent concentration-dependent dilation, and the dilation was inhibited by removal of the endothelium and by catalase, a H(2)O(2)-metabolizing enzyme. Fluorescence ROS assays showed that 4α-PDD increased the production of mitochondrial superoxide in HCAECs. 4α-PDD also enhanced the production of H(2)O(2) and superoxide in HCAs. Finally, we found that flow-induced dilation of HCAs was markedly inhibited by different TRPV4 antagonists and TRPV4-specific small interfering RNA. In conclusion, the endothelial TRPV4 channel is critically involved in flow-mediated dilation of HCAs. TRPV4-mediated Ca(2+) entry may be an important signaling event leading to the flow-induced release of mitochondrial ROS in HCAs. Elucidation of this novel TRPV4-ROS pathway may improve our understanding of the pathogenesis of coronary artery disease and/or other cardiovascular disorders.
MeSH term(s)	Aged ; Arterioles/physiology ; Atrial Appendage/cytology ; Calcium/metabolism ; Calcium Signaling/physiology ; Cells, Cultured ; Coronary Circulation/physiology ; Endothelial Cells/cytology ; Endothelial Cells/physiology ; Female ; Humans ; Male ; Middle Aged ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Phenanthridines/pharmacology ; RNA, Small Interfering/pharmacology ; Reactive Oxygen Species/metabolism ; TRPV Cation Channels/agonists ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism ; Vasodilation/physiology
Chemical Substances	5-(6'-triphenylphosphoniumhexyl)-5,6-dihydro-6-phenyl-3,8-phenanthridinediammine ; Phenanthridines ; RNA, Small Interfering ; Reactive Oxygen Species ; TRPV Cation Channels ; TRPV4 protein, human ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00717.2011
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Article: Ebselen reduces nitration and restores voltage-gated potassium channel function in small coronary arteries of diabetic rats.

Bubolz, Aaron H / Wu, Qingping / Larsen, Brandon T / Gutterman, David D / Liu, Yanping

American journal of physiology. Heart and circulatory physiology

2007 Volume 293, Issue 4, Page(s) H2231–7

Abstract: Small coronary arteries (SCA) from diabetic rats exhibit enhanced peroxynitrite (ONOO(-)) formation and concurrent impairment of voltage-dependent potassium (K(v)) channel function. However, it is unclear whether ONOO(-) plays a causative role in this ... ...

Abstract	Small coronary arteries (SCA) from diabetic rats exhibit enhanced peroxynitrite (ONOO(-)) formation and concurrent impairment of voltage-dependent potassium (K(v)) channel function. However, it is unclear whether ONOO(-) plays a causative role in this impairment. We hypothesized that functional loss of K(v) channels in coronary smooth muscle cells (SMC) in diabetes is due to ONOO(-) with subsequent tyrosine nitration of K(v) channel proteins. Diabetic rats and nondiabetic controls were treated with or without ebselen (Eb) for 4 wk. SCA were prepared for immunohistochemistry (IHC), immunoprecipitation (IP) followed by Western blot (WB), videomicroscopy, and patch-clamp analysis. IHC revealed excess ONOO(-) in SCA from diabetic rats. IP and WB revealed elevated nitration of the K(v)1.2 alpha-subunit and reduced K(v)1.2 protein expression in diabetic rats. Each of these changes was improved in Eb-treated rats. Protein nitration and K(v)1.5 expression were unchanged in SCA from diabetic rats. Forskolin, a direct cAMP activator that induces K(v)1 channel activity, dilated SCA from nondiabetic rats in a correolide (Cor; a selective K(v)1 channel blocker)-sensitive fashion. Cor did not alter the reduced dilation to forskolin in diabetic rats; however, Eb partially restored the Cor-sensitive component of dilation. Basal K(v) current density and response to forskolin were improved in smooth muscle cells from Eb-treated DM rats. We conclude that enhanced nitrosative stress in diabetes mellitus contributes to K(v)1 channel dysfunction in the coronary microcirculation. Eb may be beneficial for the therapeutic treatment of vascular complications in diabetes mellitus.
MeSH term(s)	Adenylyl Cyclases/metabolism ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Azoles/pharmacology ; Azoles/therapeutic use ; Colforsin/pharmacology ; Coronary Vessels/drug effects ; Coronary Vessels/enzymology ; Coronary Vessels/metabolism ; Coronary Vessels/physiopathology ; Cyclic AMP/metabolism ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/physiopathology ; Dose-Response Relationship, Drug ; Enzyme Activators/pharmacology ; Kv1.2 Potassium Channel/drug effects ; Kv1.2 Potassium Channel/metabolism ; Kv1.5 Potassium Channel/drug effects ; Kv1.5 Potassium Channel/metabolism ; Male ; Membrane Potentials/drug effects ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiopathology ; Organoselenium Compounds/pharmacology ; Organoselenium Compounds/therapeutic use ; Oxidative Stress/drug effects ; Peroxynitrous Acid/metabolism ; Potassium Channel Blockers/pharmacology ; Protein Subunits ; Rats ; Rats, Sprague-Dawley ; Research Design ; Triterpenes/pharmacology ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism ; Vasodilation/drug effects
Chemical Substances	Antioxidants ; Azoles ; Enzyme Activators ; Kcna2 protein, rat ; Kcna5 protein, rat ; Kv1.2 Potassium Channel ; Kv1.5 Potassium Channel ; Organoselenium Compounds ; Potassium Channel Blockers ; Protein Subunits ; Triterpenes ; correolide ; Peroxynitrous Acid (14691-52-2) ; Colforsin (1F7A44V6OU) ; 3-nitrotyrosine (3604-79-3) ; ebselen (40X2P7DPGH) ; Tyrosine (42HK56048U) ; Cyclic AMP (E0399OZS9N) ; Adenylyl Cyclases (EC 4.6.1.1)
Language	English
Publishing date	2007-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00717.2007
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Article ; Online: TRPV4-mediated endothelial Ca2+ influx and vasodilation in response to shear stress.

Mendoza, Suelhem A / Fang, Juan / Gutterman, David D / Wilcox, David A / Bubolz, Aaron H / Li, Rongshan / Suzuki, Makoto / Zhang, David X

American journal of physiology. Heart and circulatory physiology

2009 Volume 298, Issue 2, Page(s) H466–76

Abstract: The transient receptor potential vallinoid type 4 (TRPV4) channel has been implicated in the endothelial shear response and flow-mediated dilation, although the precise functions of this channel remain poorly understood. In the present study, we ... ...

Abstract	The transient receptor potential vallinoid type 4 (TRPV4) channel has been implicated in the endothelial shear response and flow-mediated dilation, although the precise functions of this channel remain poorly understood. In the present study, we investigated the role of TRPV4 in shear stress-induced endothelial Ca(2+) entry and the potential link between this signaling response and relaxation of small resistance arteries. Using immunohistochemical analysis and RT-PCR, we detected strong expression of TRPV4 protein and mRNA in the endothelium in situ and endothelial cells freshly isolated from mouse small mesenteric arteries. The selective TRPV4 agonist GSK1016790A increased endothelial Ca(2+) and induced potent relaxation of small mesenteric arteries from wild-type (WT) but not TRPV4(-/-) mice. Luminal flow elicited endothelium-dependent relaxations that involved both nitric oxide and EDHFs. Both nitric oxide and EDHF components of flow-mediated relaxation were markedly reduced in TRPV4(-/-) mice compared with WT controls. Using a fura-2/Mn(2+) quenching assay, shear was observed to produce rapid Ca(2+) influx in endothelial cells, which was markedly inhibited by the TRPV4 channel blocker ruthenium red and TRPV4-specific short interfering RNA. Flow elicited a similar TRPV4-mediated Ca(2+) entry in HEK-293 cells transfected with TRPV4 channels but not in nontransfected cells. Collectively, these data indicate that TRPV4 may be a potential candidate of mechanosensitive channels in endothelial cells through which the shear stimulus is transduced into Ca(2+) signaling, leading to the release of endothelial relaxing factors and flow-mediated dilation of small resistance arteries.
MeSH term(s)	Animals ; Biomechanical Phenomena ; Calcium/metabolism ; Calcium Signaling/physiology ; Cell Line ; Endothelium, Vascular/metabolism ; Humans ; Kidney/cytology ; Kidney/metabolism ; Leucine/analogs & derivatives ; Leucine/pharmacology ; Male ; Mesenteric Arteries/metabolism ; Mice ; Mice, Knockout ; Models, Animal ; Nitric Oxide/metabolism ; Stress, Mechanical ; Sulfonamides/pharmacology ; TRPV Cation Channels/agonists ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism ; Transfection ; Vasodilation/physiology
Chemical Substances	N-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamide ; Sulfonamides ; TRPV Cation Channels ; Trpv4 protein, mouse ; Nitric Oxide (31C4KY9ESH) ; Leucine (GMW67QNF9C) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2009-12-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00854.2009
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Article: Peroxynitrite reduces the endothelium-derived hyperpolarizing factor component of coronary flow-mediated dilation in PECAM-1-knockout mice.

Liu, Yanping / Bubolz, Aaron H / Shi, Yang / Newman, Peter J / Newman, Debra K / Gutterman, David D

American journal of physiology. Regulatory, integrative and comparative physiology

2005 Volume 290, Issue 1, Page(s) R57–65

Abstract: Platelet endothelial cell adhesion molecule 1 (PECAM-1) is capable of transducing signals in endothelial cells exposed to shear; however, the biological consequences of this signal transduction are unknown. Because shear stress elicits flow-mediated ... ...

Abstract	Platelet endothelial cell adhesion molecule 1 (PECAM-1) is capable of transducing signals in endothelial cells exposed to shear; however, the biological consequences of this signal transduction are unknown. Because shear stress elicits flow-mediated dilation (FMD), we examined whether steady-state FMD in mouse coronary arteries (MCAs) is affected in the PECAM-1 knockout (KO) mouse. MCAs were isolated from wild-type (WT) or KO mice and prepared for videomicroscopy, histofluorescence, Western blotting, and immunohistochemistry. FMD was examined in the absence and presence of N(omega)-nitro-l-arginine methyl ester (l-NAME) and l-NAME+indomethacin (INDO). FMD was reduced in KO relative to WT MCAs, but the l-NAME-inhibitable portion of FMD was similar between the two. The INDO-sensitive component of FMD was diminished in KO MCAs. In contrast, the residual component of dilation, presumably because of endothelium-derived hyperpolarizing factor (EDHF), was abolished in KO MCAs. Histofluorescence showed relatively more superoxide (O2-.; oxy-ethidium fluorescence) and peroxide production (dihydrochlorofluorescene fluoresecence) in KO MCAs at rest. Flow augmented O2-. and peroxide production in WT MCAs but had little effect on KO MCAs. Enhanced nitric oxide generation was observed in arteries from KO mice, accompanied with increased eNOS S1177 phosphorylation. In vessels from KO mice, treatment with ebselen decreased peroxynitrite (ONOO-) formation and improved the reduced FMD, largely due to restoration of the presumed EDHF component. These results suggest that PECAM-1 is necessary for normal FMD in the mouse coronary circulation. In the absence of this adhesion and signaling molecule, ONOO- production is increased concomitant with a reduction in both the EDHF and INDO-sensitive components of FMD.
MeSH term(s)	Animals ; Azoles/pharmacology ; Biological Factors/metabolism ; Coronary Vessels/metabolism ; Gene Deletion ; Hydrogen Peroxide/metabolism ; Indomethacin/pharmacology ; Male ; Mice ; Mice, Knockout ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism ; Organoselenium Compounds/pharmacology ; Peroxynitrous Acid/metabolism ; Platelet Endothelial Cell Adhesion Molecule-1/genetics ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; Prostaglandins/metabolism ; Tyrosine/metabolism ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Azoles ; Biological Factors ; Organoselenium Compounds ; Platelet Endothelial Cell Adhesion Molecule-1 ; Prostaglandins ; endothelium-dependent hyperpolarization factor ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; ebselen (40X2P7DPGH) ; Tyrosine (42HK56048U) ; Hydrogen Peroxide (BBX060AN9V) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2005-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00424.2005
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Article: Nitration and functional loss of voltage-gated K+ channels in rat coronary microvessels exposed to high glucose.

Li, Hongwei / Gutterman, David D / Rusch, Nancy J / Bubolz, Aaron / Liu, Yanping

Diabetes

2004 Volume 53, Issue 9, Page(s) 2436–2442

Abstract: ... in HG (23 mmol/l) compared with normal glucose (5.5 mmol/l) for 24 h correlated with the nitration of K ... by scavenging ONOO(-). Finally, RSCAs that were exposed to HG for 24 h showed a loss of K(v) channel dilator ...

Abstract	Coronary microvessels generate reactive oxygen species in response to high glucose (HG), resulting in vasodilator defects involving an impaired function of vascular K(+) channels. Inhibition of voltage-gated K(+) (K(v)) channels by peroxynitrite (ONOO(-)), formed by the interaction of superoxide and nitric oxide, may contribute to impaired dilation. The present study investigated whether HG induces ONOO(-) formation to mediate nitration and impairment of K(v) channels in rat small coronary arteries (RSCAs). Exposure to ONOO(-) reduced the dilator influence of K(v) channels in RSCAs. Patch-clamp studies revealed that ONOO(-) diminished whole-cell and unitary K(v) currents attributable to the K(v)1 gene family in smooth muscle cells. Subsequently, immunohistochemically detected enhancement of nitrotyrosine residues in RSCAs that were cultured in HG (23 mmol/l) compared with normal glucose (5.5 mmol/l) for 24 h correlated with the nitration of K(v)1.2 channel alpha-subunits. HG-induced nitrotyrosine formation was partially reversed by scavenging ONOO(-). Finally, RSCAs that were exposed to HG for 24 h showed a loss of K(v) channel dilator influence that also was partially restored by the ONOO(-) scavengers urate and ebselen. We conclude that ONOO(-) generated by HG impairs K(v) channel function in coronary microvessels, possibly by nitrating tyrosine residues in the pore-forming region of the K(v) channel protein.
MeSH term(s)	Animals ; Azoles/pharmacology ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Free Radical Scavengers/pharmacology ; Glucose/pharmacology ; Male ; Membrane Potentials/drug effects ; Microcirculation/drug effects ; Nitrogen/metabolism ; Organoselenium Compounds/pharmacology ; Patch-Clamp Techniques ; Peroxynitrous Acid/metabolism ; Potassium Channels, Voltage-Gated/metabolism ; Rats ; Rats, Sprague-Dawley ; Uric Acid/pharmacology ; Vasodilation/drug effects
Chemical Substances	Azoles ; Free Radical Scavengers ; Organoselenium Compounds ; Potassium Channels, Voltage-Gated ; Peroxynitrous Acid (14691-52-2) ; Uric Acid (268B43MJ25) ; ebselen (40X2P7DPGH) ; Glucose (IY9XDZ35W2) ; Nitrogen (N762921K75)
Language	English
Publishing date	2004-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/diabetes.53.9.2436
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Article ; Online: Transient receptor potential vanilloid type 4-deficient mice exhibit impaired endothelium-dependent relaxation induced by acetylcholine in vitro and in vivo.

Zhang, David X / Mendoza, Suelhem A / Bubolz, Aaron H / Mizuno, Atsuko / Ge, Zhi-Dong / Li, Rongshan / Warltier, David C / Suzuki, Makoto / Gutterman, David D

Hypertension (Dallas, Tex. : 1979)

2009 Volume 53, Issue 3, Page(s) 532–538

Abstract: Agonist-induced Ca2+ entry is important for the synthesis and release of vasoactive factors in endothelial cells. The transient receptor potential vanilloid type 4 (TRPV4) channel, a Ca2+-permeant cation channel, is expressed in endothelial cells and ... ...

Abstract	Agonist-induced Ca2+ entry is important for the synthesis and release of vasoactive factors in endothelial cells. The transient receptor potential vanilloid type 4 (TRPV4) channel, a Ca2+-permeant cation channel, is expressed in endothelial cells and involved in the regulation of vascular tone. Here we investigated the role of TRPV4 channels in acetylcholine-induced vasodilation in vitro and in vivo using the TRPV4 knockout mouse model. The expression of TRPV4 mRNA and protein was detected in both conduit and resistance arteries from wild-type mice. In small mesenteric arteries from wild-type mice, the TRPV4 activator 4alpha-phorbol-12,13-didecanoate increased endothelial [Ca2+]i in situ, which was reversed by the TRPV4 blocker ruthenium red. In wild-type animals, acetylcholine dilated small mesenteric arteries that involved both NO and endothelium-derived hyperpolarizing factors. In TRPV4-deficient mice, the NO component of the relaxation was attenuated and the endothelium-derived hyperpolarizing factor component was largely eliminated. Compared with their wild-type littermates, TRPV4-deficient mice demonstrated a blunted endothelial Ca2+ response to acetylcholine in mesenteric arteries and reduced NO release in carotid arteries. Acetylcholine (5 mg/kg, IV) decreased blood pressure by 37.0+/-6.2 mm Hg in wild-type animals but only 16.6+/-2.7 mm Hg in knockout mice. We conclude that acetylcholine-induced endothelium-dependent vasodilation is reduced both in vitro and in vivo in TRPV4 knockout mice. These findings may provide novel insight into mechanisms of Ca2+ entry evoked by chemical agonists in endothelial cells.
MeSH term(s)	Acetylcholine/pharmacology ; Animals ; Blood Pressure/drug effects ; Calcium Signaling/drug effects ; Carotid Arteries/drug effects ; Carotid Arteries/metabolism ; Disease Models, Animal ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Enzyme Inhibitors/pharmacology ; Hypertension/metabolism ; Male ; Mesenteric Arteries/drug effects ; Mesenteric Arteries/metabolism ; Mice ; Mice, Knockout ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism ; RNA, Messenger/metabolism ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism ; Vasodilation/drug effects ; Vasodilator Agents/pharmacology
Chemical Substances	Enzyme Inhibitors ; RNA, Messenger ; TRPV Cation Channels ; Trpv4 protein, mouse ; Vasodilator Agents ; Nitric Oxide (31C4KY9ESH) ; Acetylcholine (N9YNS0M02X) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2009-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.108.127100
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