Resistance arteries show the intrinsic property to constrict in response to an elevated intraluminal blood pressure, which is known as arterial myogenic tone. Whereas the underlying signaling cascade is extensively evaluated, the molecular identity of the mechanosensory elements remains elusive. A subgroup of G-protein coupled receptors (GPCRs) coupling to G_q/11-proteins is suggested to have sensory functions by recent studies at the cellular level. An array of G_q/11-coupled receptors, such as angiotensin II AT_1B, vasopressin V_1A, endothelin ET_A and ET_B and a_1A adrenoceptor, was found to be significantly enriched in resistance vessels by determining individual GPCR-mRNA-expression levels in functional pairs of resistance and conduit vessels. Pharmacological blockage of those highly expressed receptors suppressed myogenic tone in isolated murine mesenteric arteries ex vivo. Analyzing the vascular response of AT_1A^-/- mice with and without additional blocking of AT_1B receptors by candesartan suggested that especially AT_1B receptors play a dominant role for mechanosensitivity in mice. This was affirmed by investigating the myogenic response of AT_1B^-/- mice. Our results indicate that AT_1B receptors are centrally involved in the development of myogenic tone in mesenteric arteries.