Hemoglobin α in the blood vessel wall

Butcher, Joshua T.; Johnson, Troy A.; Beers, Jody M.; Columbus, Linda; Isakson, Brant E.

doi:10.1016/j.freeradbiomed.2014.04.019

Cited by 38 publications

(41 citation statements)

References 75 publications

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“…The most recently characterized inhibitory protein partner of eNOS in the microcirculation is alpha globin 25, 26 . As discussed below, NO bioavailability is decreased by alpha globin expressed in a polarized region of the microvascular endothelial cell known as the myoendothelial junction (MEJ).…”

Section: Enos Structure Co-factors and Phosphorylationmentioning

confidence: 99%

“…This observation is supported by recent research identifying the alpha subunit of hemoglobin (alpha globin) in EC 93 and noting its enrichment at MEJs. Alpha globin is a potent scavenger of NO, and in ECs, the oxidation state of its heme dictates either NO diffusion into the SMCs or irreversible NO scavenging 26, 94 . eNOS was also found to be enriched at the MEJ and forms a macromolecular complex with alpha globin 25, 94, 95 .…”

Section: Using No or Ros For Vasodilationmentioning

confidence: 99%

“…In the regulation of vascular tone, alpha globin acts in two ways: as a scavenger of NO in the MEJ 26 , and as a direct inhibitor of eNOS comparable to Cav1 93, 157, 159 . Evidence for the direct inhibition of eNOS comes from co-immunoprecipitation of alpha globin and eNOS 25 .…”

Section: Possible Pharmacological Intervention For No In the Microcirmentioning

confidence: 99%

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Endothelial nitric oxide synthase in the microcirculation

Shu

Keller

Begandt

et al. 2015

Cell. Mol. Life Sci.

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105

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Endothelial nitric oxide synthase (eNOS, NOS3) is responsible for producing nitric oxide (NO) - a key molecule that can directly (or indirectly) act as a vasodilator and anti-inflammatory mediator. In this review, we examine the structural effects of regulation of the eNOS enzyme, including post-translational modifications and subcellular localization. After production, NO diffuses to surrounding cells with a variety of effects. We focus on the physiological role of NO and NO-derived molecules, including microvascular effects on vessel tone and immune response. Regulation of eNOS and NO action is complicated; we address endogenous and exogenous mechanisms of NO regulation with a discussion of pharmacological agents used in clinical and laboratory settings and a proposed role for eNOS in circulating red blood cells.

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Section: Enos Structure Co-factors and Phosphorylationmentioning

confidence: 99%

Section: Using No or Ros For Vasodilationmentioning

confidence: 99%

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Endothelial nitric oxide synthase in the microcirculation

Shu

Keller

Begandt

et al. 2015

Cell. Mol. Life Sci.

Self Cite

105

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“…It is known that NO plays a lesser role in acetylcholine-induced vasodilation in the resistance arteries as compared to conduit arteries [36, 98–100], however this apparent difference cannot be explained by the lack of eNOS expression in the resistance arteries compared to conduits [101, 102]. Rather, it is well established that endothelial derived hyperpolarizing factor (EDHF) is the major vasodilator in the microcirculation [98].…”

Section: No and Its Role In Vascular Tone And Reactivitymentioning

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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“…However, the few studies conducted in humans have yielded inconsistent results. Whereas 1 review suggested that α + thalassemic individuals have moderate hypotension, other investigators have found elevated BPs in subjects with this condition . These studies were limited by small sample sizes and the failure to use 24‐hour ambulatory blood pressure monitoring (ABPM) to measure BP.…”

Section: Introductionmentioning

confidence: 99%

Blood Pressure and Arterial Stiffness in Kenyan Adolescents With α ⁺ Thalassemia

Etyang

Khayeka–Wandabwa

Kapesa

et al. 2017

JAHA

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BackgroundRecent studies have discovered that α‐globin is expressed in blood vessel walls where it plays a role in regulating vascular tone. We tested the hypothesis that blood pressure (BP) might differ between normal individuals and those with α+thalassemia, in whom the production of α‐globin is reduced.Methods and ResultsThe study was conducted in Nairobi, Kenya, among 938 adolescents aged 11 to 17 years. Twenty‐four‐hour ambulatory BP monitoring and arterial stiffness measurements were performed using an arteriograph device. We genotyped for α+thalassemia by polymerase chain reaction. Complete data for analysis were available for 623 subjects; 223 (36%) were heterozygous (−α/αα) and 47 (8%) were homozygous (−α/−α) for α+thalassemia whereas the remaining 353 (55%) were normal (αα/αα). Mean 24‐hour systolic BP ±SD was 118±12 mm Hg in αα/αα, 117±11 mm Hg in −α/αα, and 118±11 mm Hg in −α/−α subjects, respectively. Mean 24‐hour diastolic BP ±SD in these groups was 64±8, 63±7, and 65±8 mm Hg, respectively. Mean pulse wave velocity (PWV)±SD was 7±0.8, 7±0.8, and 7±0.7 ms−1, respectively. No differences were observed in PWV and any of the 24‐hour ambulatory BP monitoring‐derived measures between those with and without α+thalassemia.ConclusionsThese data suggest that the presence of α+thalassemia does not affect BP and/or arterial stiffness in Kenyan adolescents.

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Hemoglobin α in the blood vessel wall

Cited by 38 publications

References 75 publications

Endothelial nitric oxide synthase in the microcirculation

Endothelial nitric oxide synthase in the microcirculation

Compartmentalized nitric oxide signaling in the resistance vasculature

Blood Pressure and Arterial Stiffness in Kenyan Adolescents With α ⁺ Thalassemia

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Hemoglobin α in the blood vessel wall

Cited by 38 publications

References 75 publications

Endothelial nitric oxide synthase in the microcirculation

Endothelial nitric oxide synthase in the microcirculation

Compartmentalized nitric oxide signaling in the resistance vasculature

Blood Pressure and Arterial Stiffness in Kenyan Adolescents With α + Thalassemia

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Product

Resources

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Blood Pressure and Arterial Stiffness in Kenyan Adolescents With α ⁺ Thalassemia