Amplification of the COX/TXS/TP receptor pathway enhances uridine diphosphate-induced contraction by advanced glycation end products in rat carotid arteries

Matsumoto, Takayuki; Kojima, Mihoka; Takayanagi, Keisuke; Katome, Tomoki; Taguchi, Kumiko; Kobayashi, Tsuneo

doi:10.1007/s00424-019-02330-y

Cited by 11 publications

(6 citation statements)

References 61 publications

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“…UDP induces contraction in the aortas, coronary arteries, and mesenteric arteries of mice [31][32][33] and in the intrapulmonary arteries and carotid arteries of rat. 34,35) By contrast, UDP induces relaxation in the aorta and abdominal aorta of mice, 31,36,37) and the aortas of rats. 15) In our previous study using deoxycorticosterone acetate-salt hypertensive rats (vs. control uninephrectomized rat), femoral artery contractions induced by UDP were increased in hypertensive rat.…”

Section: Resultsmentioning

confidence: 97%

Differential Contractile Reactivity to Nucleotides in Femoral Arteries of OLETF and LETO Rats

Matsumoto

Takayanagi

Kojima

et al. 2020

Biological & Pharmaceutical Bulletin

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Extracellular nucleotides play an important role in the regulation of vascular function, and an abnormal vascular function is an important participant in the development and progression of diabetic vascular complications. The purpose of this study was to determine whether contractile responses induced by extracellular nucleotides and a dinucleotide, uridine adenosine tetraphosphate (Up 4 A), in femoral arteries would be altered at the chronic stage of type 2 diabetes. We determined the changes in contractile reactivity induced by ATP, uridine triphosphate (UTP), uridine diphosphate (UDP), and Up 4 A in the femoral arteries of Otsuka Long-Evans Tokushima Fatty (OLETF) rats (aged male type 2 diabetic rats) and, Long-Evans Tokushima Otsuka (LETO) rats (controls for OLETF rats). ATP-induced contractions were greater in OLETF rats than in LETO rats. UTP-induced contractions were lower in OLETF rats than in LETO rats. UDP-and Up 4 Ainduced contractions were similar between OLETF and LETO rats. The femoral artery contractile changes induced by the extracellular nucleotides and dinucleotide were similar when nitric oxide synthase was inhibited. These results suggest that the extent of femoral artery contractile reactivity to nucleotides/dinucleotides differs during long-term duration of type 2 diabetes.

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Section: Resultsmentioning

confidence: 97%

Differential Contractile Reactivity to Nucleotides in Femoral Arteries of OLETF and LETO Rats

Matsumoto

Takayanagi

Kojima

et al. 2020

Biological & Pharmaceutical Bulletin

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“…In SHR femoral arteries, we previously suggested that enhancement of noradrenaline-induced contractions was partly due to increased COX-derived prostanoids [25]. Actually, there are several reports suggesting that uridine nucleotides can produce prostanoids in various cells and vessels [11, 45]. Although both endothelial and vascular smooth muscle cells are sources of prostanoids, contractions were still greater in endothelium-denuded femoral arteries of SHR than in those from WKY.…”

Section: Discussion/conclusionmentioning

confidence: 99%

“…There are several conflicting evidences suggesting that UDP or UTP causes vasocontraction and vasorelaxation. For example, UDP causes vasocontraction in the mouse aorta [14], mouse mesenteric artery [18], rat pulmonary and intrapulmonary arteries [13, 19], rat basilar artery [9, 33], and rat carotid artery [11], and vasorelaxation in mouse aorta [14] mouse abdominal aorta [15], and rat aorta [11, 16]. UTP also causes vasocontraction in rat intrapulmonary artery [19], rat basilar artery [9, 33], rat aorta [9, 34], and vasorelaxation in rat aorta [10] and mouse aorta [35, 36].…”

Section: Discussion/conclusionmentioning

confidence: 99%

Extracellular Uridine Nucleotides-Induced Contractions Were Increased in Femoral Arteries of Spontaneously Hypertensive Rats

Matsumoto¹,

Takayanagi²,

Katome³

et al. 2021

Pharmacology

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Introduction: Femoral arterial dysfunction including abnormal vascular responsiveness to endogenous ligands was often seen in arterial hypertension. Extracellular nucleotides including uridine 5′-diphosphate (UDP) and uridine 5′-triphosphate (UTP) play important roles for homeostasis in the vascular system including controlling the vascular tone. However, responsiveness to UDP and UTP in femoral arteries under arterial hypertension remains unclear. The aim of this study was to investigate if hypertension has an effect of vasoconstrictive responsiveness to UDP and UTP in femoral arteries of spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs) after 7 and 12 months old. Methods: Organ baths were conducted to determine vascular reactivity in isolated femoral arterial rings. Results: In femoral arteries obtained from 12-month-old rats, augmented contractile responses to UDP and UTP were seen in femoral arteries of SHR than in those of WKY under situations not only intact but also nitric oxide synthase inhibition, whereas no difference of extracellular potassium-induced vasocontraction was seen in both SHR and WKY groups. Similar contraction trends occurred in femoral arteries obtained from 7-month-old rats. Moreover, contractions induced by UDP and UTP were increased in endothelium-denuded arteries. Cyclooxygenase inhibition decreased the contractions induced by these nucleotides and abolished the differences in responses between the SHR and WKY groups. Conclusions: This study demonstrates the importance of regulation of extracellular uridine nucleotides-induced contractions in hypertension-associated peripheral arterial diseases.

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“…The negative inflammatory and protein cross-linking effects of AGEs could explain this damage to the common carotid artery [11]. AGEs also contribute to endothelial dysfunction by inducing vasoconstriction through endothelin-1 and reducing vasodilatation via depletion of nitric oxide [11,38,39]. Besides, hyperglycemia mediated AGEs excessive accumulation leads to extracellular matrix damage and a decline in several enzymatic activities [40].…”

Section: Accumulation Of Ages In Diabetes Mellitus Damage Cardiomyocymentioning

confidence: 99%

The cardiovascular complications of diabetes: a striking link through protein glycation

Ahmad

Farah

Al-Qirim

2020

Romanian Journal of Internal Medicine

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Diabetes mellitus is a predominant cause of mortality and morbidity worldwide. One of its serious health problems is cardiovascular complications. Advanced glycation end products (AGEs) are a group of heterogeneous toxic oxidant compounds that are formed after a nonenzymatic reaction between monosaccharides and free amino groups of proteins, compound lipids, and nucleic acids. AGE interacts with various types of cells through a receptor for AGE (RAGE). The interaction between AGE and RAGE is responsible for a cascade of inflammation, oxidative stress, and disruption of calcium homeostasis in cardiac cells of diabetic patients. There is striking evidence that the AGE/RAGE axis with its consequences on inflammation and oxidative stress plays a major role in the development of cardiovascular complications. Therefore, considering AGE as a therapeutic target with foreseeable results would be a wise direction for future research. Interestingly, several studies on nutraceutical, pharmaceutical, and natural products have begun to reveal promising therapeutic results, and this could lead to better health outcomes for many diabetic patients worldwide. This article discusses the current literature addressing the connection between protein glycation and diabetes cardiovascular complications and suggests future avenues of research.

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Amplification of the COX/TXS/TP receptor pathway enhances uridine diphosphate-induced contraction by advanced glycation end products in rat carotid arteries

Cited by 11 publications

References 61 publications

Differential Contractile Reactivity to Nucleotides in Femoral Arteries of OLETF and LETO Rats

Differential Contractile Reactivity to Nucleotides in Femoral Arteries of OLETF and LETO Rats

Extracellular Uridine Nucleotides-Induced Contractions Were Increased in Femoral Arteries of Spontaneously Hypertensive Rats

The cardiovascular complications of diabetes: a striking link through protein glycation

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