Nitric oxide (NO) is a ubiquitous, volatile, cellular signaling molecule that operates across a wide physiological concentration range (pM-µM) in different tissues. It is a highly diffusible messenger and intermediate in various metabolic pathways. NO plays a pivotal role in maintaining optimum cardiovascular function, particularly by regulating vascular tone and blood flow. This review highlights the need for accurate, real-time bioimaging of NO in clinical diagnostic, therapeutic, monitoring, and theranostic applications within the cardiovascular system. We summarize electrochemical, optical, and nanoscale sensors that allow measurement and imaging of NO, both directly and indirectly via surrogate measurements. The physical properties of NO render it difficult to accurately measure in tissues using direct methods. There are also significant limitations associated with the NO metabolites used as surrogates to indirectly estimate NO levels. All these factors added to significant variability in the measurement of NO using available methodology have led to a lack of sensors and imaging techniques of clinical applicability in relevant vascular pathologies such as atherosclerosis and ischemic heart disease. Challenges in applying current methods to biomedical and clinical translational research, including the wide physiological range of NO and limitations due to the characteristics and toxicity of the sensors are discussed, as are potential targets and modifications for future studies. The development of biocompatible nanoscale sensors for use in combination with existing clinical imaging modalities provides a feasible opportunity for bioimaging NO within the cardiovascular system.

Cardiovascular bioimaging of nitric oxide: Achievements, challenges, and the future

https://lup.lub.lu.se/search/ws/files/1703788/4437311.pdf

Low density lipoprotein induces upregulation of vasoconstrictive endothelin type B receptor expression.

Homocysteine regulates endothelin type B receptors in vascular smooth muscle cells

Homocysteine up-regulates endothelin type A receptor in vascular smooth muscle cells through Sirt1/ERK1/2 signaling pathway.

https://lup.lub.lu.se/search/ws/files/2534818/4588616.pdf

Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Minimally modified low-density lipoprotein (mmLDL) is a risk factor for cardiovascular disease. The present study investigated the effects of mmLDL on the expression of endothelin type A () receptors in coronary arteries. Rat coronary arteries were organ-cultured for 24&#x2009;h. The contractile responses were recorded using a myographic system. receptor mRNA and protein expressions were determined using real-time PCR and western blotting, respectively. The results showed that organ-culturing in the presence of mmLDL enhanced the arterial contractility mediated by the receptor in a concentration-dependent and time-dependent manner. Culturing with mmLDL (10&#x2009;&#x3bc;g/mL) for 24&#x2009;h shifted the concentration-contractile curves toward the left significantly with increased of from control of and significantly increased receptor mRNA and protein levels. Inhibition of the protein kinase C, extracellular signal-related kinases 1 and 2 (ERK1/2), or NF-&#x3ba;B activities significantly attenuated the effects of mmLDL. The c-Jun N-terminal kinase inhibitor or the p38 pathway inhibitor, however, had no such effects. The results indicate that mmLDL upregulates the receptors in rat coronary arterial smooth muscle cells mainly via activating protein kinase C, ERK1/2, and the downstream transcriptional factor, NF-&#x3ba;B.

/pdf/minimally-modified-ldl-upregulates-endothelin-type-a-19uvv29b6i.pdf

Minimally modified LDL upregulates endothelin type A receptors in rat coronary arterial smooth muscle cells.

Minimally modified low-density lipoprotein (mmLDL) is a well-known risk factor for cardiovascular diseases. The present study was designed to investigate the role of mmLDL in the endothelium-dependent

Minimally Modified LDL-Induced Impairment of Endothelium-Dependent Relaxation in Small Mesenteric Arteries of Mice.

This study is to investigate the impairment and possible mechanism of endothelium-dependent relaxation of mice mesenteric arteries induced by mmLDL. Wire myography was employed to examine endothelial function of mesenteric arteries. Ultramicrostructure of mesenteric vascular beds were detected by transmission electron microscope. The results showed that endothelium cell edema and peeling, vascular elastic membrane fracture traces in mmLDL group. Endothelium-dependent relaxation was decreased in a time-dependent and dose-dependent manner by using mmLDL, compared with normal arteries. In endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the Rmax and pIC50 were decreased from (63 +/- 5) % and 6.42 +/- 0.09 of normal saline control to (31 +/- 3) % and 5.67 +/- 0.07 in mmLDL group (P < 0.001, P < 0.001), respectively. In nitric oxide (NO)-mediated relaxation, the Rmax and pIC50 were decreased from (45 +/- 4) % and 5.93 +/- 0.08 in normal saline control to (32 +/- 4) % and 5.43 +/- 0.11 in mmLDL group (P < 0.05, P < 0.01), respectively. There is no significant alteration of prostacyclin I2 (PGI2) pathway between these two groups. In conclusion, mmLDL induced the impairment of the ultramicrostructure of mesenteric vascular endothelium cell as well as the endothelium-dependent relaxation. The latter includes the dysfunction of NO- and EDHF pathway mediated endothelium-dependent relaxation.

[Minimally modified LDL induced impairment of endothelium-dependent relaxation in mesenteric arteries of mice].

The invention discloses the reactivity of a colon cancer artery to a vasoconstrictive medium. An alpha receptor and an ETA receptor are main vasoconstrictive receptors of a normal artery, and the vasoconstrictive action of the alpha receptor and the ETA receptor of the colon cancer artery is obviously weaker than that of a cancer peripheral artery. The maximal contraction and the half-maximal effect concentration of normal artery contraction caused by noradrenaline (NA) are respectively 97%+/-19% and 5.94+/-0.17, Emax and pEC50 of the NA contraction of the colon cancer artery are respectively 74%+/-5% and 5.54+/-0.21, and Emax and pEC50 of the contraction of the cancer peripheral artery are respectively 119%+/-11% and 5.84+/-0.09.

Reactivity of colon cancer artery to vasoconstrictive medium

The invention discloses a method for raising an ETB (endothelin type B) receptor of a brain basilar artery based on mmLDL (minimally modified low density lipoprotein). The method comprises the following steps: carrying out co-culture on a rat brain basilar artery and mmLDL for 24 hours; adding a corresponding signal transduction pathway inhibitor when a signal transduction pathway is investigated; determining microvessel tension by virtue of a muscle tension pantograph; and respectively detecting the mRNA level and the protein level by using real-time PCR (polymerase chain reaction) and Western blot. The result shows that a fresh brain basilar artery loop ETB receptor does not contract in a mediated manner basically; ETB receptor-mediated contraction is significantly increased by organ culture; the contracting dose-effect curve moves towards the left; meanwhile, Emax reaches 88+/-6%; the contracting dose-effect curve further moves towards the left by co-culture of 10mu g/ml of mmLDL; Emax reaches 116+/-12%; and the mmLDL is capable of raising the brain basilar artery ETB receptor by activating PKC (protein kinase C), MAPK (mitogen-activated protein kinase) and the NF-kB (transcription factor nuclear factor-kappaB) signal transduction pathway.

Method for raising ETB (endothelin type B) receptor of brain basilar artery based on mmLDL (minimally modified low density lipoprotein)

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