Endothelial dysfunction and improvement of the angiotensin II-reactivity in hypercholesterolemic rabbits: Role of cyclooxygenase metabolites

Jerez, Susana; Sierra, Liliana; Coviello, Alfredo; Bruno, María Peral de

doi:10.1016/j.ejphar.2007.10.037

Cited by 17 publications

(31 citation statements)

References 29 publications

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“…In previous works we characterized a model of hypercholesterolemia by feeding rabbits on a high cholesterol diet (HD) by 6 weeks. This model shows hyperlipidemia (Medina et al 2014), increase of oxidative stress and inflammatory markers (Karbiner et al 2013) and vascular dysfunction accompanied by reduction of acetylcholine relaxation and increase of angiotensin II reactivity (Jerez et al 2008). Recently, we demonstrate in vitro beneficial effects of hydroalcoholic Z. punctata extract (ZpE) and its major flavonoids on vascular function in hypercholesterolemic rabbits (Roco et al 2017).…”

Section: Introductionmentioning

confidence: 93%

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Oral administration of Zuccagnia punctata extract improves lipid profile, reduces oxidative stress and prevents vascular dysfunction in hypercholesterolemic rabbits

et al. 2018

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Section: Introductionmentioning

confidence: 93%

“…Endothelial dysfunction caused by lipotoxicity is mediated through several mechanisms that include increased oxidative stress and pro-inflammatory responses. Impairment of endothelium-dependent vasodilation and reduction of nitric oxide (NO) availability are the main manifestations of such condition (Jerez et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Oral administration of Zuccagnia punctata extract improves lipid profile, reduces oxidative stress and prevents vascular dysfunction in hypercholesterolemic rabbits

et al. 2018

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“…ROS, in turn, react with and inactivate NO (20). However, Jerez et al (12) showed that the NSAID indomethacin improved endothelium-dependent aortic ring relaxation, while blocking angiotensin II-reactivity in hypercholesterolemic rabbits. Inhibition of the renin-angiotensin pathway by NSAID treatment likely contributes to the reduction in oxidative stress and improvement in microvessel relaxation that we observed in this study.…”

Section: Discussionmentioning

confidence: 99%

Effects of cyclooxygenase inhibition on cardiovascular function in a hypercholesterolemic swine model of chronic ischemia

Chu

Robich

Bianchi

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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T, Sellke FW. Effects of cyclooxygenase inhibition on cardiovascular function in a hypercholesterolemic swine model of chronic ischemia. Am J Physiol Heart Circ Physiol 302: H479 -H488, 2012. First published October 28, 2011 doi:10.1152/ajpheart.00146.2011The cardiovascular effects of cyclooxygenase (COX) inhibition remain controversial, especially in the setting of cardiovascular comorbidities. We examined the effects of nonselective and selective COX inhibition on cardiovascular function in a hypercholesterolemic swine model of chronic ischemia. Twenty-four intact male Yorkshire swine underwent left circumflex ameroid constrictor placement and were subsequently given either no drug (HCC; n ϭ 8), a nonselective COX inhibitor (440 mg/day naproxen; HCNS; n ϭ 8), or a selective COX-2 inhibitor (200 mg/day celecoxib; HCCX; n ϭ 8). After 7 wk, myocardial functional was measured and myocardium from the nonischemic ventricle and ischemic area-at-risk (AAR) were analyzed. Regional function as measured by segmental shortening was improved in the AAR of HCCX compared with HCC. There was no significant difference in perfusion to the nonischemic ventricle between groups, but myocardial perfusion in the AAR was significantly improved in the HCCX group compared with controls at rest and during pacing. Endothelium-dependent microvessel relaxation was diminished by ischemia in HCC animals, but both naproxen and celecoxib improved vessel relaxation in the AAR compared with controls, and also decreased the vasoconstrictive response to serotonin. Thromboxane levels in the AAR were decreased in both HCNS and HCCX compared with HCC, whereas prostacyclin levels were decreased only in HCNS, corresponding to a decrease in prostacyclin synthase expression. Chronic ischemia increased apoptosis in Troponin T negative cells and intramyocardial fibrosis, both of which were reduced by celecoxib administration in the AAR. Capillary density was decreased in both the HCNS and HCCX groups. Protein oxidative stress was decreased in both HCNS and HCCX, whereas lipid oxidative stress was decreased only in the HCCX group. Thus nonselective and especially selective COX inhibition may have beneficial myocardial effects in the setting of hypercholesterolemia and chronic ischemia. Whether these effects modulate cardiovascular risk in patients taking these drugs remains to be seen, but evidence to date suggests that they do not. cholesterol; myocardial ischemia; perfusion; prostaglandins NONSTEROIDAL ANTI-INFLAMMATORY drugs (NSAIDs) function by inhibiting the conversion of arachadonic acid into prostaglandin H 2 by cyclooxygenase (COX), inhibiting the production of a family of prostanoids that includes prostacyclin and thromboxane. Unfortunately, the gastrointestinal side effects of

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“…Enhanced activation of TP receptors and augmented endothelium-and TP receptor-dependent vascular contractions are also observed in various metabolic diseases and experimental models of diabetes and hypercholesterolemia (Traupe et al, 2002;Jerez et al, 2008;Michel et al, 2008b).…”

Section: Vasoconstrictor Prostanoid-mediated Signalling In Vascular Smentioning

confidence: 96%

“…Enhanced activation of TP receptors and augmented endothelium‐ and TP receptor‐dependent vascular contractions are also observed in various metabolic diseases and experimental models of diabetes and hypercholesterolemia (Traupe et al ., ; Jerez et al ., ; Michel et al ., ). Increased U46619‐induced contractions are seen in arteries from obese and diabetic animals (Nobe et al ., ; Yang et al ., ; Baretella et al ., ; Matsumoto et al ., ).…”

Section: Vasoconstrictor Prostanoid‐mediated Signalling In Vascular Smentioning

confidence: 97%

Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes

Matsumoto

Goulopoulou

Taguchi

et al. 2015

British J Pharmacology

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Vascular dysfunction plays a pivotal role in the development of systemic complications associated with arterial hypertension and diabetes. The endothelium, or more specifically, various factors derived from endothelial cells tightly regulate vascular function, including vascular tone. In physiological conditions, there is a balance between endothelium-derived factors, that is, relaxing factors (endothelium-derived relaxing factors; EDRFs) and contracting factors (endothelium-derived contracting factors; EDCFs), which mediate vascular homeostasis. However, in disease states, such as diabetes and arterial hypertension, there is an imbalance between EDRF and EDCF, with a reduction of EDRF signalling and an increase of EDCF signalling. Among EDCFs, COX-derived vasoconstrictor prostanoids play an important role in the development of vascular dysfunction associated with hypertension and diabetes. Moreover, uridine adenosine tetraphosphate (Up4A), identified as an EDCF in 2005, also modulates vascular function. However, the role of Up4A in hypertension-and diabetes-associated vascular dysfunction is unclear. In the present review, we focused on experimental and clinical evidence that implicate these two EDCFs (vasoconstrictor prostanoids and Up4A) in vascular dysfunction associated with hypertension and diabetes. Abbreviations AA, arachidonic acid; AICAR, 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside; AMPK, AMP-activated protein kinase; CDK2, cyclin-dependent kinase 2; cPLA2, cytosolic PLA2; DOCA, deoxycorticosterone-acetate; E2, 17β-oestradiol; ECs, endothelial cells; EDCF, endothelium-derived contracting factor; EDHF, endothelium-derived hyperpolarizing factor; EDRF, endothelium-derived relaxing factor; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; ET-1, endothelin-1; GK, Goto-Kakizaki; GPER, G protein-coupled oestrogen receptor; HETEs, hydroxyeicosatetraenoic acid; HO-1, haem oxygenase-1; HUVEC, human umbilical vein endothelial cells; L-NAME, N G -nitro-l-arginine methyl ester; L-PGDS, lipocalin-type PGD synthase; MLC20, myosin light chain 20; NO, nitric oxide; NSAIDs, non-steroidal anti-inflammatory drugs; OLETF, Otsuka Long-Evans Tokushima Fatty; OPN, osteopontin; PDGFR, platelet-derived growth factor receptor; PGI2, prostacyclin; PGIS, prostacyclin synthase; ROCK, Rho kinase; ROS, reactive oxygen species; S6K, S6 kinase; SHR, spontaneously hypertensive rats; SMCs, smooth muscle cells; STZ, streptozotocin; TP, TxA2/endoperoxide receptor; TxA2, thromboxane A2; TxS, thromboxane synthase; Up4A, uridine adenosine tetraphosphate; VP, vasopressin; WKY, Wistar-Kyoto ratsThe endothelium plays a pivotal role in the regulation of vascular tone (Vapaatalo and Mervaala, 2001;Pries and Kuebler, 2006;Flammer and Luscher, 2010;Toda et al., 2010;Flammer et al., 2012; Favero et al., 2014). In response to mechanical forces (e.g. shear stress) and endogenous ligands, endothelial cells (ECs) release a diversity of factors that mediate or directly induce vascular smooth muscle contraction or relaxation (Vapaatalo and Me...

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Endothelial dysfunction and improvement of the angiotensin II-reactivity in hypercholesterolemic rabbits: Role of cyclooxygenase metabolites

Cited by 17 publications

References 29 publications

Oral administration of Zuccagnia punctata extract improves lipid profile, reduces oxidative stress and prevents vascular dysfunction in hypercholesterolemic rabbits

Oral administration of Zuccagnia punctata extract improves lipid profile, reduces oxidative stress and prevents vascular dysfunction in hypercholesterolemic rabbits

Effects of cyclooxygenase inhibition on cardiovascular function in a hypercholesterolemic swine model of chronic ischemia

Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes

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