Microvascular Endothelial Dysfunction and Enhanced Thromboxane and Endothelial Contractility in Patients with HIV

Wang, Dan; Melancon, J. Keith; Verbesey, Jennifer E.; Liu, Chenglong; Aslam, Shakil; Young, Mary; Wilcox, Christopher S.

doi:10.4172/2155-6113.1000267

Cited by 19 publications

(14 citation statements)

References 55 publications

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“…The endothelial dysfunction observed in HIV‐infected patients is explained best by an increase microvascular production of ROS, thereby reducing NO bioavailability, blunting acetylcholine‐induced endothelium‐dependent relaxation, facilitating endothelium‐dependent contractions and enhancing TP receptor responsiveness (Wang et al . ).…”

Section: Endothelium‐dependent Contractionsmentioning

confidence: 97%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

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The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monophosphate (cGMP) initiating relaxation. The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDH-mediated responses). As regards the latter, hydrogen peroxide (H O ) now appears to play a dominant role. Endothelium-dependent relaxations involve both pertussis toxin-sensitive G (e.g. responses to α -adrenergic agonists, serotonin, and thrombin) and pertussis toxin-insensitive G (e.g. adenosine diphosphate and bradykinin) coupling proteins. New stimulators (e.g. insulin, adiponectin) of the release of EDRFs have emerged. In recent years, evidence has also accumulated, confirming that the release of NO by the endothelial cell can chronically be upregulated (e.g. by oestrogens, exercise and dietary factors) and downregulated (e.g. oxidative stress, smoking, pollution and oxidized low-density lipoproteins) and that it is reduced with ageing and in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and EDH, in particular those due to H O ), endothelial cells also can evoke contraction of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factors. Recent evidence confirms that most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells and that prostacyclin plays a key role in such responses. Endothelium-dependent contractions are exacerbated when the production of nitric oxide is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive and diabetic patients. In addition, recent data confirm that the release of endothelin-1 can contribute to endothelial dysfunction and that the peptide appears to be an important contributor to vascular dysfunction. Finally, it has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate (cIMP) rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle.

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Section: Endothelium‐dependent Contractionsmentioning

confidence: 97%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

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“…Recent studies identify maternal hypertension as the most important risk factor for adverse birth outcomes among HIV-infected women on ART both epidemiologically and at placental examination [7,15,38, 95]. Women with chronic HIV infection on ART have underlying endothelial dysfunction [96] that may be exacerbated by the stress of pregnancy and lead to systemic hypertension, poor placentation and placental insufficiency. An important modulator of endothelial function in pregnancy is progesterone [97] and recent data suggest an association between ART and low progesterone resulting in adverse birth outcomes [98,99] (potentially connected by decreased prolactin regulation of progesterone metabolism, and mediated by a shift away from progesterone-induced Th-2 immunologic responses in normal pregnancy).…”

Section: 0 Expert Opinionmentioning

confidence: 99%

Surveillance monitoring for safety of in utero antiretroviral therapy exposures: current strategies and challenges

Zash

Williams

Sibiude

et al. 2016

Expert Opinion on Drug Safety

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Introduction The use of antiretroviral therapy (ART) in pregnancy to prevent vertical HIV transmission has been one of the most successful public health programs in the last decade. As a result, an unprecedented number of women are taking ART at conception and during pregnancy. Given few randomized studies evaluating safety of different ART regimens in pregnancy, ongoing drug safety surveillance is critical. Areas Covered This review aims to provide a rationale for ART drug safety surveillance, describe changing patterns of ART use and summarize current surveillance efforts in both low-resource and high-resource settings. Additionally, biostatistical approaches to and challenges in analysis of observational surveillance data are discussed. Expert Opinion The global landscape of ART use in pregnancy is rapidly increasing and evolving. Any increase in adverse effects of in-utero exposure to ART has the potential to reduce the impact of improvements in infant morbidity and mortality gained from decreased vertical HIV transmission. ART drug safety surveillance should therefore be a critical piece of programs to prevent mother to child transmission in both high- and low-resource settings. Current surveillance efforts could be strengthened with long-term follow-up of exposed children, pooling of data across cohorts and standardized approaches to analysis.

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“…Future studies evaluating endothelium-dependent vasodilation before and after treatment might be informative in this regard. 13 Lower hemoglobin was an independent risk factor for HF in this study. 9 Although part of this might have been dilutional (perhaps excess plasma volume even before clinically recognized HF), it is also possible that other contributors such as occult iron deficiency that can impair ventricular function might have been present.…”

Section: Article See P 1630mentioning

confidence: 76%

Moving Beyond Cardio-Centricity in Heart Failure Risk Stratification

Borlaug

2015

Circulation

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Microvascular Endothelial Dysfunction and Enhanced Thromboxane and Endothelial Contractility in Patients with HIV

Cited by 19 publications

References 55 publications

Endothelial dysfunction and vascular disease - a 30th anniversary update

Endothelial dysfunction and vascular disease - a 30th anniversary update

Surveillance monitoring for safety of in utero antiretroviral therapy exposures: current strategies and challenges

Moving Beyond Cardio-Centricity in Heart Failure Risk Stratification

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