Anti-lipid deposition effect of HMG-CoA reductase inhibitor, pitavastatin, in a rat model of hypertension and hypercholesterolemia

Kumai, Toshio; Oonuma, Shigeko; Matsumoto, Naoki; Takeba, Yuko; Taniguchi, Rika; Kamio, K.; Miyazu, Osamu; Koitabashi, Yu; Sekine, Susumu; Tadokoro, Mamoru; Kobayashi, Shinichi

doi:10.1016/j.lfs.2003.09.051

Cited by 21 publications

(10 citation statements)

References 30 publications

(31 reference statements)

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“…Kumai et al demonstrated that sponta-neously hypertensive hyperlipidemic rats (SHHR) treated with N G -nitro-L-arginine methyl ester (L-NAME) and a high-fat diet showed a marked deposition of lipids and thickening of the endothelium of their aortas (11). We have previously reported that SHHR has a systolic blood pressure that is higher than 150 mmHg, a plasma cholesterol concentration that is greater than 150 mg / dl, and apparent hyperfibrinogenemia (12,13).…”

Section: Introductionmentioning

confidence: 99%

“…In this study, we have attempted to develop a rat model of metabolic syndrome with an accumulation of visceral fat by feeding the SHHR a high-fat diet and sucrose solution (HFDS) after L-NAME ingestion to inactivate nitric oxide (NO). Metabolic syndrome is accelerated by atherosclerosis derived from vascular endothelial injury, and NO inactivation may contribute to the initiation and progression of atherosclerosis (11,14). So, we pretreated the SD (Sprague-Dawley) rats and SHHR with L-NAME before HFDS treatment and evaluated the pathophysiological features under the combination of hyperlipidemia, hypertension, and abnormal glucose metabolism.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Pioglitazone on Increases in Visceral Fat Accumulation and Oxidative Stress in Spontaneously Hypertensive Hyperlipidemic Rats Fed a High-Fat Diet and Sucrose Solution

et al. 2007

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Abstract. We examined oxidative stress and metabolic characteristics of the spontaneously hypertensive hyperlipidemic rat (SHHR) when it was fed a high-fat diet and sucrose solution (HFDS) after N G -nitro-L-arginine methyl ester ingestion to develop a rat model of metabolic syndrome. This study was carried out to assess the effects of pioglitazone on levels of lipid peroxide (LPO), Cu,Zn superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GPx), and non-esterified fatty acids (NEFA) in the plasma and liver tissue in HFDS-SHHR compared with Sprague-Dawley rats (SD). In the HFDS-treated groups, levels of LPO, CAT, GPx, and NEFA were elevated and levels of Cu,Zn-SOD were reduced in the plasma and liver tissue, with a marked accumulation of visceral fat. The changes induced by HFDS feeding were severe in the SHHR model that had essential hypertension and hyperlipidemia, when compared with SD that did not have these essential risk factors. Subcutaneous injection of 10 mg / kg per day of pioglitazone for 2 months significantly restored levels of LPO, CAT, GPx, Cu,Zn-SOD, and NEFA in the HFDS-SHHR group, and visceral fat accumulation was reduced. These results suggest that HFDS-SHHR is a suitable model of metabolic syndrome and that pioglitazone treatment can improve oxidative dysregulation in this rat model.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Pioglitazone on Increases in Visceral Fat Accumulation and Oxidative Stress in Spontaneously Hypertensive Hyperlipidemic Rats Fed a High-Fat Diet and Sucrose Solution

et al. 2007

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“…Moreover, invasive changes occur in the subendothelium of SHHR when nitric oxide NO production is inactivated followed by a high fat diet and sucrose water treatment SHHR-HDFS 7 . Furthermore, a previous study found visceral fat accumulation and increased oxidative stress in SHHR-HFDS 8 .…”

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confidence: 99%

Visceral Fat Accumulation is Associated with Oxidative Stress and Increased Matrix Metalloproteinase-9 Expression in Atherogenic Factor-overlapped Model Rats

Tomita¹,

Iwai²,

Kumai

et al. 2010

Showa Univ J Med Sci

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“…Moreover, plasma catecholamine levels and low-density lipoprotein expression were higher in SHHRs than in SpragueDawley (SD) rats. In the aorta, both endothelial degeneration and lipid deposits were also reported (Kumai et al, 2004). Based on these findings, we concluded that SHHR is a novel beneficial tool for application as a multiple hypertensive and hyperlipidemic model.…”

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confidence: 58%

Alterations of Glucose-Dependent and -Independent Bladder Smooth Muscle Contraction in Spontaneously Hypertensive and Hyperlipidemic Rat

Nobe

Yamazaki²,

Kumai³

et al. 2007

J Pharmacol Exp Ther

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Alteration of bladder contractility was examined in the spontaneously hypertensive and hyperlipidemic rat (SHHR; age, 9 months; systolic blood pressure, Ͼ150 mm Hg; plasma cholesterol, Ͼ150 mg/dl). Carbachol (CCh) induced time-and dose-dependent contractions in Sprague-Dawley (age-matched control) rats and SHHR; however, maximal levels differed significantly (13.3 Ϯ 2.2 and 5.4 Ϯ 1.9 N/mm 2 following 10 M CCh treatment, respectively; n ϭ 5). This difference, which was maintained in calciumreplaced physiological salt solution (PSS), was suppressed by pretreatment with rho kinase inhibitor, 1 M Y27632 [(R)-(ϩ)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide]; moreover, total activity of rho kinase was also reduced in SHHR bladder. Pretreatment of bladders under high-glucose (HG) conditions (22.2 mM glucose-contained PSS for 30 min) led to enhancement of CCh-induced contraction solely in control animals. Under HG conditions, both protein kinase C (PKC) activity and production of diacylglycerol (DG) derived from incorporated glucose declined in SHHR bladder; however, sustained elevation of plasma glucose level was not detected in SHHR. These results suggested that bladder contractility dysfunction in SHHR is attributable to alteration of rho kinase activity and the DG-PKC pathway. This dysfunction may occur prior to chronic hyperglycemia onset in progressive hypertension and hyperlipidemia.

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Anti-lipid deposition effect of HMG-CoA reductase inhibitor, pitavastatin, in a rat model of hypertension and hypercholesterolemia

Cited by 21 publications

References 30 publications

Effects of Pioglitazone on Increases in Visceral Fat Accumulation and Oxidative Stress in Spontaneously Hypertensive Hyperlipidemic Rats Fed a High-Fat Diet and Sucrose Solution

Effects of Pioglitazone on Increases in Visceral Fat Accumulation and Oxidative Stress in Spontaneously Hypertensive Hyperlipidemic Rats Fed a High-Fat Diet and Sucrose Solution

Visceral Fat Accumulation is Associated with Oxidative Stress and Increased Matrix Metalloproteinase-9 Expression in Atherogenic Factor-overlapped Model Rats

Alterations of Glucose-Dependent and -Independent Bladder Smooth Muscle Contraction in Spontaneously Hypertensive and Hyperlipidemic Rat

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