Eicosanoids and renal vascular function in diseases

Imig, John D.

doi:10.1042/cs20050251

Cited by 80 publications

(104 citation statements)

References 156 publications

(374 reference statements)

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“…Several reports have shown an impairment of acetylcholine (ACh)-induced endothelium-derived hyperpolarizing factor (EDHF)-signaling in the microvasculature of diabetic animals (Fukao et al, 1997;Makino et al, 2000;Matsumoto et al, 2003aMatsumoto et al, ,b, 2005Matsumoto et al, , 2006aFitzgerald et al, 2005). Moreover, diabetes-related endothelial dysfunction has been linked to changes in eicosanoid metabolism (Sowers and Epstein, 1995;Imig, 2006).…”

Section: Introductionmentioning

confidence: 99%

Altered arachidonic acid-mediated responses in the perfused kidney of the streptozotocin-induced diabetic rat

Kamata

Hosokawa

Matsumoto

et al. 2006

J. Smooth Muscle Res.

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Using perfused kidneys isolated from age-matched controls and streptozotocin (STZ)-induced diabetic rats, we investigated the effects of arachidonic acid (AA) on perfusion pressure in the presence of methoxamine. AA elicited a transient contraction followed by a sustained relaxation in each group. The amplitude of contraction was smaller in the diabetic group than in the control group, whereas the amplitude of the sustained relaxation was greater in the former than in the latter group. In the diabetic group, the AA-induced sustained relaxation was completely inhibited by indomethacin [cyclooxygenase (COX) inhibitor], SKF525A [cytochrome P450 (CYP450) inhibitor], or clotrimazole (epoxygenase inhibitor), but not by furegrelate [thromboxane A2 (TXA2)-synthase inhibitor], SQ29548 (TXA2-receptor antagonist), or baicalein [lipoxygenase (LOX) inhibitor]. In the diabetic kidney, more-or-less additive inhibitions of the AAinduced relaxation were seen when indomethacin was given with either SKF525A or clotrimazole. These results suggest that in the STZ-induced diabetic perfused kidney, vasorelaxant metabolites derived from AA (probably COX and/or CYP450 metabolites) are increased, and may serve to regulate vascular tone.

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Section: Introductionmentioning

confidence: 99%

Altered arachidonic acid-mediated responses in the perfused kidney of the streptozotocin-induced diabetic rat

Kamata

Hosokawa

Matsumoto

et al. 2006

J. Smooth Muscle Res.

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“…Likewise, renal complications associated with diabetes such as vascular hypertrophy and matrix deposition have been attributed to hypertension [56]. There is also evidence that adiposity independent of hypertension and diabetes is associated with increased incidence of chronic kidney disease [25,53,57]. Inflammation, oxidative stress, and lipid abnormalities that are associated with obesity are most likely contributing to the progression of renal damage.…”

Section: Renal Damage and Cardiometabolic Syndromementioning

confidence: 99%

“…There are at least two COX enzymes, COX-1 and COX-2, expressed in the kidney. COX metabolites play a critical role in renal blood flow regulation, renin generation and vascular inflammation [25,58,63]. Alterations in COX metabolites contribute to endothelial dysfunction and renal damage in diabetes [56,64,65].…”

Section: Eicosanoids As a Therapeutic Target For Renal Damage In Cardmentioning

confidence: 99%

“…Elevated blood glucose levels, hypertension and an increase in glomerular filtration (GFR) are major factors contributing to renal injury [2,25,26]. Obese individuals and obese mice have an elevated renal plasma flow and GFR that can lead to an increased glomerular capillary pressure and glomerular injury [27,28].…”

Section: Renal Damage and Cardiometabolic Syndromementioning

confidence: 99%

“…There are three distinct enzymatic pathways, cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP), that metabolize arachidonic acid. These three pathways are very important for renal function and renal damage in cardiometabolic syndrome has been attributed at least in part to eicosanoid metabolites [25,53,57] (Figure 4). …”

Section: Eicosanoids As a Therapeutic Target For Renal Damage In Cardmentioning

confidence: 99%

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Eicosanoids and renal damage in cardiometabolic syndrome

Imig

2008

Expert Opinion on Drug Metabolism & Toxicology

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Obesity, hypertension and type 2 diabetes are major contributing factors to the increase in the number of patients that have chronic kidney disease. The clustering of visceral obesity and cardiovascular risk factors has been designated metabolic syndrome or cardiometabolic syndrome. Cardiometabolic syndrome is associated with a complex systemic inflammatory state that has been implicated in medically important complications including endothelial dysfunction. Inflammation, endothelial dysfunction, and insulin resistance are interrelated and have reciprocal relationships that link cardiovascular and metabolic diseases. Ultimately, cardiometabolic syndrome increases the risk for cardiovascular events and end organ damage. Although the number of patients with cardiometabolic syndrome is escalating, therapeutic approaches have not been developed that provide protection to the kidney. Eicosanoids are altered in cardiometabolic syndrome and contribute the progression of renal injury. The anti-hypertensive and anti-inflammatory actions of epoxides and soluble epoxide hydrolase inhibitors make these attractive eicosanoid therapeutic targets for chronic kidney disease in patients with cardiometabolic syndrome. Keywordskidney; epoxyeicosatrienoic acids; epoxide hydrolase; obesity; cytokines; inflammation Cardiometabolic SyndromeIn recent years, the number of obese people in the world is growing rapidly and has reached epidemic status. Obesity is the central phenotype in metabolic syndrome, also known as cardiometabolic syndrome that clusters with other cardiovascular risk factors. These other cardiovascular risk factors include hypertension, type 2 diabetes, insulin resistance, low high-density lipoproteins (HDL) cholesterol, elevated triglycerides, microalbuminuria, and atherosclerosis [1,2,3] (Figure 1). The Adult treatment Panel II of the National Cholesterol Education Program has defined metabolic syndrome as any three of the following five traits: visceral obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and impaired fasting glucose [4]. Although obesity is the phenotypic hallmark of cardiometabolic syndrome, the other risk factors that manifest in individuals varies greatly. Blood pressure elevation in obese individuals is closely related to weight gain; however, not all obese individuals become hypertensive [5][6][7][8]. The relationship between obesity and hypertension is well established but the exact consequences to end organ damage remains unknown. Interestingly, hypertension and diabetes account for seventy percent of patients with end stage renal disease (ESRD) and the number of patients with ESRD will double in this decade [9,10]. One of the main reasons for the doubling in ESRD patients is the increase in obesity related type 2 diabetes and its co-existence with hypertension.

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Renal System

2012

Comparative Pathophysiology and Toxicology of Cyclooxygenases

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Eicosanoids and renal vascular function in diseases

Cited by 80 publications

References 156 publications

Altered arachidonic acid-mediated responses in the perfused kidney of the streptozotocin-induced diabetic rat

Altered arachidonic acid-mediated responses in the perfused kidney of the streptozotocin-induced diabetic rat

Eicosanoids and renal damage in cardiometabolic syndrome

Renal System

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