To address whether perivascular adipose is a source of endogenous vasoconstrictors that might alter the balance between relaxing and contracting factors [15], for the present study we employed not only a diet-induced obesity (DIO) model, but also a novel model of monogenic visceral obesity, the G protein-coupled estrogen receptor (GPER)-deficient mouse [16]–[20]. Here, GPER1 is linked to obesity due to melanocortin 4 receptor deficiency.