Abstract
Background: We previously reported that the adipokine chemerin, when added exogenously to the isolated rat mesenteric artery, amplified electrical field-stimulated (EFS) contraction. The Chemerin1 antagonist CCX832 alone inhibited EFS-induced contraction in tissues with but not without perivascular adipose tissue (PVAT). These data suggested indirectly that chemerin itself, presumably from the PVAT, facilitated EFS-induced contraction. We created the chemerin KO rat and now test the focused hypothesis that endogenous chemerin amplifies EFS-induced arterial contraction. Methods: The superior mesenteric artery +PVAT from global chemerin WT and KO female rats, with endothelium and sympathetic nerve intact, were mounted into isolated tissue baths for isometric and EFS-induced contraction. Results: CCX832 reduced EFS (2–20 Hz)-induced contraction in tissues from the WT but not KO rats. Consistent with this finding, the magnitude of EFS-induced contraction was lower in the tissues from the KO vs. WT rats, yet the maximum response to the adrenergic stimulus PE was not different among all tissues. Conclusion: These studies support that endogenous chemerin modifies sympathetic nerve-mediated contraction through Chemerin1, an important finding relative in understanding chemerin’s role in control of blood pressure.
Highlights
Epidemiological evidence strongly supports the positive association between circulating levels of the secreted protein and adipokine chemerin [1,2], body mass index (BMI) and blood pressure [3,4,5]
In the same electrical field-stimulated (EFS) experiment, we discovered that the Chemerin1 antagonist CCX832 [12] alone reduced EFS-induced contraction in arteries +perivascular adipose tissue (PVAT) but not in arteries –PVAT
Using Western analyses, we verified that chemerin protein in the plasma was lost in the KO but present in the WT females that were used in this experiment (Figure 1A)
Summary
Epidemiological evidence strongly supports the positive association between circulating levels of the secreted protein and adipokine chemerin [1,2], body mass index (BMI) and blood pressure [3,4,5]. Exogenous chemerin-9 amplified the sympathetic nerve-mediated electrical field-stimulated (EFS) contraction of the isolated mesenteric artery [12]. While we knew chemerin was expressed in PVAT [13], we had, at that time, no way to prove definitively that the protein chemerin, itself, was this substance These data only supported than an activated Chemerin supported EFS-induced contraction. We previously reported that the adipokine chemerin, when added exogenously to the isolated rat mesenteric artery, amplified electrical field-stimulated (EFS) contraction. Methods: The superior mesenteric artery +PVAT from global chemerin WT and KO female rats, with endothelium and sympathetic nerve intact, were mounted into isolated tissue baths for isometric and EFS-induced contraction. Conclusion: These studies support that endogenous chemerin modifies sympathetic nerve-mediated contraction through Chemerin, an important finding relative in understanding chemerin’s role in control of blood pressure
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