The perivascular adipose tissue environment plays a key role in regulating its function. How immune populations residing in adipose tissue communicate with other cells has significant implications in health and disease. We have shown that healthy perivascular adipose tissue has a relaxant effect which this is lost in obesity. In obesity, adipocytes become enlarged, hypoxic and inflamed. Immune cell profiles residing in perivascular adipose tissue become dysregulated; our data show decreased eosinophil numbers compared with control. Therefore, we further investigated the role of eosinophils in mediating normal perivascular adipose tissue function. We used wire myography to assess vascular contractility of mesenteric blood vessels (~200 micrometer diameter). Animals deficient in eosinophils demonstrated a loss of the relaxant effect of perivascular adipose tissue and had increased mean arterial pressure and blood glucose levels, similar to obese mice. This effect was independent of other immune cells. Reconstitution of eosinophils restored perivascular adipose tissue function and physiological measures. Reconstituting eosinophils derived from knockout models demonstrated that the loss of PVAT function was due to reduced bioavailability of adiponectin and adipocyte-derived nitric oxide. This effect was mediated via β3 adrenoceptors activation by catecholamines. We further identified eosinophils as a novel source of these mediators. In summary, we demonstrate that eosinophils are important regulators of healthy perivascular adipose tissue function. Our findings identify a novel therapeutic avenue for the treatment of obesity and type 2 diabetes.