Activation of TP receptors induces high release of PGI2 in coronary arteries of renal hypertensive rats

Paula, Tiago; Silva, B.R.; Grando, Marcella Daruge; Souza, Hugo Celso Dutra de; Bendhack, Lusiane Maria

doi:10.1016/j.yjmcc.2018.08.007

Cited by 6 publications

(6 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Over-production of reactive oxygen species (ROS) in the cardiovascular system triggers deficiency in vasodilation induced by nitric oxide (NO), since ROS reacts NO neutralizing its effects 5,18 . Our results show that APAP treatment increases lipid peroxidation in the vascular system, leading to impaired endothelium-dependent vasodilation by overproducing prostanoids (mostly PGD 2 ) as observed with other drugs and conditions that induce increased oxidative stress 14,16,18,19 .…”

Section: Fig 3: Effect Of Apap Treatment (N=6 For Each Group) On Vasc...supporting

confidence: 55%

“…The arteries were stimulated with Phe (0.1 μmol/L, 15 min) and the supernatant was used to quantify the levels of AA and TXB 2 , PGD 2 , 12-HETE and 15-HETE. An aliquot of each extracted sample (20 μL) was injected into an HPLC column (Accucore C18-50×3 mm, 2.6 μm; Thermo Scientific, Waltham, MA-USA) for HPLC analysis [16]. The HPLC system was directly interfaced with the electrospray source of a triple quadrupole mass spectrometer (API 4000; SCIEX, Framingham, MA), wherein MS analysis was carried out in the negative ion mode.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Untitled

2024

IJPSR

View full text Add to dashboard Cite

Acetaminophen (APAP) is the most consumed potentially toxic drug in the world, and its cardiovascular injury has been emphasized. We evaluated the role of inflammatory mediators in the impaired vascular relaxation after APAP treatment. Rats were treated with APAP for 2 weeks (400 mg/Kg/day/p.o.) and after euthanasia, blood was collected for biochemical analysis (hepatic transaminases, lipid peroxidation and glutathione), and aortas were isolated for vascular reactivity, lipid peroxidation and biochemical analysis (glutathione, arachidonic acid, TBXA 2 , PGD 2 , 12-HETE and 15-HETE). Both blood and arteries presented increased levels of lipid peroxidation and decreased levels of glutathione. The vasodilation response to acetylcholine was impaired in the APAP group and restored after treatment with diclofenac (10 μM). In the arteries, levels of arachidonic acid were reduced while PGD 2 was increased (TBXA 2 , 12-and 15-HETE remained significantly unchanged). Thus, oxidative stress and contractile prostanoids play a significant role in the impaired vascular relaxation caused by APAP treatment. INTRODUCTION:Like a widespread drug throughout the world, acetaminophen (N-acetyl-paminophenol, paracetamol; APAP) also named paracetamol, has been considered effective and relatively safe, but due to its low price and easy availability, there has been a significant increase in poisonings due to misuse and overdose 1, 2 . Lately, studies have emphasized the toxic side effects and serious complications of APAP on the cardiovascular system 3-6 .

show abstract

Section: Fig 3: Effect Of Apap Treatment (N=6 For Each Group) On Vasc...supporting

confidence: 55%

Section: Methodsmentioning

confidence: 99%

Untitled

2024

IJPSR

View full text Add to dashboard Cite

show abstract

“…Generally, TP receptors bind mainly to thromboxane TXA 2 and cause contraction of smooth muscle cells by activating G protein–coupled receptors, which in turn mobilize calcium ions in vivo 32 . Paula et al 33 showed that TP receptor activation increased PGI2 synthesis in the coronary arteries of renal hypertensive rats and that TP receptor activation enhanced the mitogenic effects of platelet-derived growth factor and increased the synthesis and release of endogenous basic fibroblast growth factor, which in turn stimulated vascular smooth muscle cell proliferation and hypertrophy. Leung 34 concluded that after functional loss of IP receptors, PGI 2 synthesis is no longer restricted by NO production, and large amounts of PGI 2 bind to TP receptors in vascular smooth muscle cells, subsequently causing an increase in intracellular calcium ion concentration in vascular smooth muscle cells, which mediates vasoconstriction via myosin light chain kinase.…”

Section: Discussionmentioning

confidence: 99%

A Study on Vascular Regulators as Early Biomarkers of Hand Arm Vibration Syndrome

Yang,

Chen,

et al. 2023

J Occup Environ Med

View full text Add to dashboard Cite

Objectives Purpose of this study was to study the changes in expression of vascular regulators after vibration exposure and during the onset of vibration-induced white finger (VWF) and to screen for Vascular Regulatory Factors that could be used as early biomarkers of HAVS. Methods Using judgmental sampling from a Chinese factory, workers with VWF and hand-transmitted vibration exposure but without VWF were selected for research. Blood samples were taken from all subjects, and the levels of nine of the vascular regulators were measured using ELISA. Results Receiver Operating Characteristic (ROC) curve analysis was performed on nine vascular regulators to assess their diagnostic sensitivity for VWF with the following area under the curve (AUC) results: PGI2 = 0.861, ANP = 0.840. Conclusion Collectively, PGI2 and ANP exhibited the most potential for the early diagnosis of HAVS.

show abstract

“…COX-2 but not COX-1 expression was higher in kidney cystic epithelial cells and in the interstitium, and mPGES1 and PGI synthase levels were increased in a mouse model of PKD and treatment with a ns-NSAID, Sulindac, resulted in retardation of cysts development (Zhang et al, 2019). Higher COX-2 expression and no changes in COX-1 expression were noted in coronary arteries of renal hypertensive rats (Paula et al, 2018). COX-2 expression, but not COX-1, is markedly decreased in the cortex and increased in the inner medulla in response to unilateral ureteral obstruction (UUO) (Chou et al, 2003) and bilateral ureteral obstruction (BUO) (Cheng et al, 2004).…”

Section: Cox-1 and Cox-2 Expression And Homeostasis In The Cardio-renal Systems In Diseasementioning

confidence: 95%

Cardio-renal safety of non-steroidal anti-inflammatory drugs

Radi

Khan

2019

J. Toxicol. Sci.

View full text Add to dashboard Cite

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used therapeutic class in clinical medicine. These are sub-divided based on their selectivity for inhibition of cyclooxygenase (COX) isoforms (COX-1 and COX-2) into: (1) non-selective (ns-NSAIDs), and (2) selective NSAIDs (s-NSAIDs) with preferential inhibition of COX-2 isozyme. The safety and pathophysiology of NSAIDs on the renal and cardiovascular systems have continued to evolve over the years following short-and long-term treatment in both preclinical models and humans. This review summarizes major learnings on cardiac and renal complications associated with pharmaceutical inhibition of COX-1 and COX-2 with focus on preclinical to clinical translatability of cardio-renal data.

show abstract

Activation of TP receptors induces high release of PGI2 in coronary arteries of renal hypertensive rats

Cited by 6 publications

References 54 publications

Untitled

Untitled

A Study on Vascular Regulators as Early Biomarkers of Hand Arm Vibration Syndrome

Cardio-renal safety of non-steroidal anti-inflammatory drugs

Contact Info

Product

Resources

About