Nitric Oxide Signaling in the Microcirculation

Buerk, Donald G.; Barbee, Kenneth A.; Jaron, Dov

doi:10.1615/critrevbiomedeng.v39.i5.40

Cited by 34 publications

(28 citation statements)

References 236 publications

(279 reference statements)

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“…Its major physiological functions include dilating vascular smooth muscle, and inhibiting the aggregation of platelets, platelet and leukocyte adhesion and hyperplasia of the vascular smooth muscle (18,19). Hormones can damage vascular endothelial cells in which NO is produced and inhibit the activity of NO synthase (NOS).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide content and apoptosis rate in steroid-induced avascular necrosis of the femoral head

Bai

Liu

Zhao

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to explore the effect on nitric oxide (NO) content and osteocyte apoptosis of steroid-induced avascular necrosis of the femoral head (SANFH) in an animal model of SANFH. A total of 40 Japanese white rabbits, 5 months of age and weighing 2.5±0.5 kg, were randomly divided into groups A (hormone + endotoxin group), B (endotoxin + normal saline group), C (normal saline + hormone group) and D (control group). Following the establishment of the model, a blood sample was taken from the heart of each animal and centrifuged; the levels of NO in the serum were detected. The bilateral femoral heads were conventionally dissected, fixed, decalcified and stained with hematoxylin and eosin. Subsequently, the empty bone lacunae were counted under an optical microscope. Changes in osteocyte morphology were observed using electron microscopy and osteocyte apoptosis was detected with a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The percentage of empty bone lacunae in group A was significantly higher compared with that in groups B, C and D (P<0.01); however, there was no significant difference in percentage among groups B, C and D. The NO content in group A was significantly higher compared with that in groups B, C and D (P<0.01); however, there was no significant difference in NO content among groups B, C and D. The osteocyte apoptosis index in group A was significantly higher compared with that in the other groups (P<0.01); there was no significant difference among groups B, C and D. NO content was positively correlated with osteocyte apoptosis index (r=0.707). Thus, the present study found that NO content and the osteocyte apoptosis index were increased in SANFH, and that they play an important role in SANFH. The content of NO was positively correlated with the osteocyte apoptosis index, indicating that NO induces apoptosis.

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Section: Discussionmentioning

confidence: 99%

Nitric oxide content and apoptosis rate in steroid-induced avascular necrosis of the femoral head

Bai

Liu

Zhao

et al. 2015

Experimental and Therapeutic Medicine

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“…While NO quickly diffuses away from eNOS to reach its targets, there appears to be a system in place to regulate the amount of NO capable of traversing the cell membrane as models of unregulated diffusion do not consistently account for the biochemistry of eNOS-dependent signaling [6, 94]. Work by Straub et al showed that hemoglobin α (Hbα) is present at the MEJ and acts to regulate NO passage.…”

Section: The Myoendothelial Junction and No Signalingmentioning

confidence: 99%

“…NO is a short-lived molecule with diverse biological functions. Thought to evolutionarily precede both the presence of oxygen in the atmosphere and the development of heme-containing proteins, NO is a ubiquitous signaling molecule [6]. It plays an important role in neurotransmission [7, 8], regulation of vascular tone and vasodilation [9, 10], and regulation of both gene transcription [11, 12] and mRNA translation [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Compartmentalized nitric oxide signaling in the resistance vasculature

Mutchler¹,

Straub

2015

Nitric Oxide

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Nitric oxide (NO) was first described as a bioactive molecule through its ability to stimulate soluble guanylate cyclase, but the revelation that NO was the endothelium derived relaxation factor drove the field to its modern state. The wealth of research conducted over the past 30 years has provided us with a picture of how diverse NO signaling can be within the vascular wall, going beyond simple vasodilation to include such roles as signaling through protein S-nitrosation. This expanded view of NO’s actions requires highly regulated and compartmentalized production. Importantly, resistance arteries house multiple proteins involved in the production and transduction of NO allowing for efficient movement of the molecule to regulate vascular tone and reactivity. In this review, we focus on the many mechanisms regulating NO production and signaling action in the vascular wall, with a focus on the control of endothelial nitric oxide synthase (eNOS), the enzyme responsible for synthesizing most of the NO within these confines. We also explore how cross talk between the endothelium and smooth muscle in the microcirculation can modulate NO signaling, illustrating that this one small molecule has the capability to produce a plethora of responses.

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“…Thus, any potential time delay between the onset of CFL variation and NO/O 2 responses was not considered. Buerk et al (2011) previously reported that acute changes in the WSS over short time periods may not be sufficient to induce changes in the eNOS expression. In a separate study, Andrews et al (2010) performed measurements of the shear stressinduced NO production from endothelial cells in a flow chamber.…”

Section: Potential Limitations Of the Current Studymentioning

confidence: 99%