scholarly journals Negative News: Cl− and HCO3− in the Vascular Wall

Physiology ◽  
2016 ◽  
Vol 31 (5) ◽  
pp. 370-383 ◽  
Author(s):  
Ebbe Boedtkjer ◽  
Vladimir V. Matchkov ◽  
Donna M. B. Boedtkjer ◽  
Christian Aalkjaer

Cl− and HCO3− are the most prevalent membrane-permeable anions in the intra- and extracellular spaces of the vascular wall. Outwardly directed electrochemical gradients for Cl− and HCO3− permit anion channel opening to depolarize vascular smooth muscle and endothelial cells. Transporters and channels for Cl− and HCO3− also modify vascular contractility and structure independently of membrane potential. Transport of HCO3− regulates intracellular pH and thereby modifies the activity of enzymes, ion channels, and receptors. There is also evidence that Cl− and HCO3− transport proteins affect gene expression and protein trafficking. Considering the extensive implications of Cl− and HCO3− in the vascular wall, it is critical to understand how these ions are transported under physiological conditions and how disturbances in their transport can contribute to disease development. Recently, sensing mechanisms for Cl− and HCO3− have been identified in the vascular wall where they modify ion transport and vasomotor function, for instance, during metabolic disturbances. This review discusses current evidence that transport (e.g., via NKCC1, NBCn1, Ca2+-activated Cl− channels, volume-regulated anion channels, and CFTR) and sensing (e.g., via WNK and RPTPγ) of Cl− and HCO3− influence cardiovascular health and disease.

Author(s):  
Ashley Dawson ◽  
Yidan Wang ◽  
Yanming Li ◽  
Scott A. LeMaire ◽  
Ying H. Shen

Endothelial cells (ECs) are vital for blood vessel integrity and have roles in maintaining normal vascular function, healing after injury, and vascular dysfunction. Extensive phenotypic heterogeneity has been observed among ECs of different types of blood vessels in the normal and diseased vascular wall. Although ECs with different phenotypes can share common functions, each has unique features that may dictate a fine-tuned role in vascular health and disease. Recent studies performed with single-cell technology have generated powerful information that has significantly improved our understanding of EC biology. Here, we summarize a variety of EC types, states, and phenotypes recently identified by using new, increasingly precise techniques in transcriptome analysis.


2021 ◽  
Vol 8 ◽  
Author(s):  
Karen Julissa Loaeza-Reyes ◽  
Edgar Zenteno ◽  
Adriana Moreno-Rodríguez ◽  
Rafael Torres-Rosas ◽  
Liliana Argueta-Figueroa ◽  
...  

The cardiovascular system is a complex and well-organized system in which glycosylation plays a vital role. The heart and vascular wall cells are constituted by an array of specific receptors; most of them are N- glycosylated and mucin-type O-glycosylated. There are also intracellular signaling pathways regulated by different post-translational modifications, including O-GlcNAcylation, which promote adequate responses to extracellular stimuli and signaling transduction. Herein, we provide an overview of N-glycosylation and O-glycosylation, including O-GlcNAcylation, and their role at different levels such as reception of signal, signal transduction, and exogenous molecules or agonists, which stimulate the heart and vascular wall cells with effects in different conditions, like the physiological status, ischemia/reperfusion, exercise, or during low-grade inflammation in diabetes and aging. Furthermore, mutations of glycosyltransferases and receptors are associated with development of cardiovascular diseases. The knowledge on glycosylation and its effects could be considered biochemical markers and might be useful as a therapeutic tool to control cardiovascular diseases.


Physiology ◽  
2006 ◽  
Vol 21 (2) ◽  
pp. 134-145 ◽  
Author(s):  
Kurt R. Stenmark ◽  
Neil Davie ◽  
Maria Frid ◽  
Evgenia Gerasimovskaya ◽  
Mita Das

An increasing volume of experimental data indicates that the adventitial fibroblast, in both the pulmonary and systemic circulations, is a critical regulator of vascular wall function in health and disease. A rapidly emerging concept is that the vascular adventitia acts as biological processing center for the retrieval, integration, storage, and release of key regulators of vessel wall function. In response to stress or injury, resident adventitial cells can be activated and reprogrammed to exhibit different functional and structural behaviors. In fact, under certain conditions, the adventitial compartment may be considered the principal injury-sensing tissue of the vessel wall. In response to vascular stresses such as overdistension and hypoxia, the adventitial fibroblast is activated and undergoes phenotypic changes, which include proliferation, differentiation, upregulation of contractile and extracellular matrix proteins, and release of factors that directly affect medial smooth muscle cell tone and growth and that stimulate recruitment of inflammatory and progenitor cells to the vessel wall. Each of these changes in fibroblast phenotype modulates either directly or indirectly changes in overall vascular function and structure. The purpose of this review is to present the current evidence demonstrating that the adventitial fibroblast acts as a key regulator of pulmonary vascular function and structure from the “outside-in.”


Heart ◽  
2018 ◽  
Vol 104 (20) ◽  
pp. 1654-1662 ◽  
Author(s):  
Jennifer Mancio ◽  
Evangelos K Oikonomou ◽  
Charalambos Antoniades

Adipose tissue (AT) is no longer viewed as a passive, energy-storing depot, and a growing body of evidence supports the concept that both quantitative and qualitative aspects of AT are critical in determining an individual’s cardiometabolic risk profile. Among all AT sites, perivascular AT (PVAT) has emerged as a depot with a distinctive biological significance in cardiovascular disease given its close anatomical proximity to the vasculature. Recent studies have suggested the presence of complex, bidirectional paracrine and vasocrine signalling pathways between the vascular wall and its PVAT, with far-reaching implications in cardiovascular diagnostics and therapeutics. In this review, we first discuss the biological role of PVAT in both cardiovascular health and disease, highlighting its dual pro-atherogenic and anti-atherogenic roles, as well as potential therapeutic targets in cardiovascular disease. We then review current evidence and promising new modalities on the non-invasive imaging of epicardial AT and PVAT. Specifically, we present how our expanding knowledge on the bidirectional interplay between the vascular wall and its PVAT can be translated into novel clinical diagnostics tools to assess coronary inflammation. To this end, we present the example of a new CT-based method that tracks spatial changes in PVAT phenotype to extract information about the inflammatory status of the adjacent vasculature, highlighting the numerous diagnostic and therapeutic opportunities that arise from our increased understanding of PVAT biology.


2012 ◽  
Vol 2 (2) ◽  
pp. 113-118
Author(s):  
Maiara Marx Luz Fiusa ◽  
Joyce Maria Annichino-Bizzacchi ◽  
Erich Vinicius De Paula

2021 ◽  
Vol 22 (5) ◽  
pp. 2298
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain

The renin-angiotensin-aldosterone system (RAAS) is implicated in hypertension and kidney disease. The developing kidney can be programmed by various early-life insults by so-called renal programming, resulting in hypertension and kidney disease in adulthood. This theory is known as developmental origins of health and disease (DOHaD). Conversely, early RAAS-based interventions could reverse program processes to prevent a disease from occurring by so-called reprogramming. In the current review, we mainly summarize (1) the current knowledge on the RAAS implicated in renal programming; (2) current evidence supporting the connections between the aberrant RAAS and other mechanisms behind renal programming, such as oxidative stress, nitric oxide deficiency, epigenetic regulation, and gut microbiota dysbiosis; and (3) an overview of how RAAS-based reprogramming interventions may prevent hypertension and kidney disease of developmental origins. To accelerate the transition of RAAS-based interventions for prevention of hypertension and kidney disease, an extended comprehension of the RAAS implicated in renal programming is needed, as well as a greater focus on further clinical translation.


2021 ◽  
Vol 22 (13) ◽  
pp. 6933
Author(s):  
Yuqi Wu ◽  
Chong-Zhi Wang ◽  
Jin-Yi Wan ◽  
Haiqiang Yao ◽  
Chun-Su Yuan

The gut microbiota exists throughout the full life cycle of the human body, and it has been proven to have extensive impacts on health and disease. Accumulating evidence demonstrates that the interplay between gut microbiota and host epigenetics plays a multifaceted role in health maintenance and disease prevention. Intestinal microflora, along with their metabolites, could regulate multiple epigenetic pathways; e.g., DNA methylation, miRNA, or histone modification. Moreover, epigenetic factors can serve as mediators to coordinate gut microbiota within the host. Aiming to dissect this interplay mechanism, the present review summarizes the research profile of gut microbiota and epigenetics in detail, and further interprets the biofunctions of this interplay, especially the regulation of intestinal inflammation, the improvement of metabolic disturbances, and the inhibition of colitis events. This review provides new insights into the interplay of epigenetics and gut microbiota, and attempts to reveal the mysteries of health maintenance and disease prevention from this new perspective.


2009 ◽  
Vol 84 (9) ◽  
pp. 822-830 ◽  
Author(s):  
Nisha Charkoudian ◽  
Jennifer A. Rabbitts

2008 ◽  
Vol 101 (10) ◽  
pp. S75-S86 ◽  
Author(s):  
Bradley J. Willcox ◽  
J. David Curb ◽  
Beatriz L. Rodriguez

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