Impairment of vasodilation and effects of perivascular adipose tissue in metabolic syndrome

Kagota, Satomi; Maruyama, Kana; Iwata, Saki; Tada, Yasuyuki

doi:10.1254/fpj.145.59

Cited by 2 publications

(1 citation statement)

References 27 publications

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“…MetS is a chronic condition which worsens with time and thus, requires long-term strategies for clinical treatment. Our previous studies show that mesenteric PVAT has compensatory effects to maintain vascular tonus under the condition of impaired NO-mediated relaxations in SHRSP.ZF (at 20 wks), i.e., PVAT enhances vasodilation in response to either endothelium-derived NO induced by acetylcholine or exogenous NO derived from sodium nitroprusside in mesenteric artery of SHRSP.ZF [4,30,31]. However, the compensatory function of PVAT was impaired at a later stage of MetS (at 30 wks).…”

Section: Discussionmentioning

confidence: 99%

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl–l-Cysteine-Sensitive Factor(s)

Kagota

Maruyama‐Fumoto

Iwata

et al. 2018

IJMS

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Perivascular adipose tissue (PVAT) can regulate vascular tone. In mesenteric arteries of SHRSP.Z-Leprfa/IzmDmcr rats (SHRSP.ZF) with metabolic syndrome, vascular dysfunction is compensated by PVAT-dependent mechanisms that disappear with increasing age. In this study, we investigated the mechanisms of the age-related changes and responsible factor(s) involved in the enhancing effects of mesenteric arterial PVAT in SHRSP.ZF. Acetylcholine- and sodium nitroprusside-induced relaxations of isolated arteries were greater with PVAT than without PVAT at 17 and 20 weeks of age (wks), and as expected, this enhancement by the presence of PVAT disappeared at 23 wks. PVAT mRNA levels of angiotensin II type 1 (AT1) receptor-associated protein was less and AT1 receptor was unchanged at 23 wks when compared to 20 wks. At 20 wks, the enhanced acetylcholine-induced relaxation by the presence of PVAT was inhibited by N-acetyl-l-cysteine (NAC). Acetylcholine-induced relaxation of arteries without PVAT was increased in the presence of exogenously added apelin. PVAT mRNA level of apelin was higher in SHRSP.ZF than in control Wistar-Kyoto rats, and the level was decreased with aging. These results suggest that AT1 receptor activation in PVAT, and changes in the regulation of apelin and a NAC-sensitive factor are related to the age-dependent deterioration of the vasodilation enhancing effects of mesenteric arterial PVAT in SHRSP.ZF.

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Section: Discussionmentioning

confidence: 99%

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl–l-Cysteine-Sensitive Factor(s)

Kagota

Maruyama‐Fumoto

Iwata

et al. 2018

IJMS

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Functional Relationship between Arterial Tissue and Perivascular Adipose Tissue in Metabolic Syndrome

Kagota

Iwata²,

Maruyama³

et al. 2016

YAKUGAKU ZASSHI

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Metabolic syndrome is a complex of disorders that includes visceral obesity, insulin resistance, hypertension, and dyslipidemia. It is characterized by an increased risk for serious cardiovascular events. Adipocytes are now recognized to contribute to the development of cardiovascular complications in metabolic syndrome via the release of several bioactive substances (adipocytokines). Obesity induces an increase in the volume of perivascular adipose tissue (PVAT), which is located outside the blood vessels. In recent years, PVAT has been reported to produce/release vasoactive adipocytokines. Thus, PVAT can modulate vasomotor function by releasing vasorelaxing/vasocontracting factors, resulting in the development of cardiovascular disease due to metabolic syndrome. By using animal models (SHR/ NDmcr-cp rats, SHRSP.Z-Lepr fa /IzmDmcr rats, and B6.BKS (D)-Lepr fa /J mice), we have demonstrated that chronic oxidative-nitrative stress is closely linked to the development of vascular dysfunction in response to nitric oxide (NO) in resistant arteries with increasing age/exposure to metabolic abnormalities. Further, our recentˆndings have led us to believe that PVAT helps in the regulation of vasodilation to compensate for the impaired vasodilation observed in pathophysiological conditions in the mesenteric arteries of SHRSP.Z-Lepr fa /IzmDmcr rats. However, a breakdown of the compensatory system occurs with long-term exposure to metabolic abnormalities. We propose the concept of the functional regulation of vascular tissue by PVAT in metabolic syndrome.

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Impairment of vasodilation and effects of perivascular adipose tissue in metabolic syndrome

Cited by 2 publications

References 27 publications

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl–l-Cysteine-Sensitive Factor(s)

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl–l-Cysteine-Sensitive Factor(s)

Functional Relationship between Arterial Tissue and Perivascular Adipose Tissue in Metabolic Syndrome

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