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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Perivascular adipose tissue (PVAT) modulates the vascular tone. We previously demonstrated that mesenteric arterial PVAT enhances vasodilation in SHRSP.Z-Leprfa/IzmDmcr (SHRSP.ZF) rats. However, the factors involved in the vasodilation effect of PVAT have not been identified. Therefore, this study aimed to determine whether apelin, an adipokine, is involved in mediating the beneficial effects of PVAT. We pre-treated mesenteric arterial segments from SHRSP.ZF rats with apelin before observing the vascular activities. Compared to controls without PVAT, apelin significantly enlarged vasodilation in response to acetylcholine; the result was similar to the response observed when PVAT is present. In contrast, the same trend in vasodilation was not observed in response to sodium nitroprusside. Additionally, when apelin was cumulatively administered to segments without PVAT from Wistar-Kyoto rats, vasorelaxation was not induced. These results suggest that apelin acts as a vasodilative enhancer under the condition of endothelial nitric oxide (NO) synthesis. Apelin may, therefore, be involved in mediating the beneficial effect of PVAT via a possible increase in NO production in metabolic syndrome.