Predominant α2-adrenoceptor control of chelonian systemic resistance arteries provides a mechanistic basis for the cardiovascular effects of α2-agonist sedation.

Chelonians are commonly sedated with α2-adrenoceptor agonists, such as medetomidine, and bradycardia is consistently reported following administration. This may reflect a baroreflex response to α2-mediated peripheral vasoconstriction and increased systemic vascular resistance, but the vascular contribution to these cardiovascular effects has not been directly investigated. Here, we tested the hypothesis that α2-adrenoceptors contribute predominantly to vascular contraction in chelonians, contrasting with the α1-adrenoceptor-dominant regulation described in mammals. Mesenteric resistance arteries from three chelonian species spanning two chelonian families (Stigmochelys pardalis, Mauremys reevesii, and Mauremys sinensis) were studied using wire myography. Concentration-response curves were generated for the nonselective α-adrenoceptor agonist noradrenaline, the selective α1-adrenoceptor agonist methoxamine, and the α2-adrenoceptor agonists medetomidine, detomidine, xylazine, and romifidine. The effects of α2-adrenoceptor antagonism with vatinoxan and α1-adrenoceptor antagonism with prazosin were also assessed. Medetomidine and detomidine produced robust, concentration-dependent vasoconstriction, whereas xylazine and romifidine produced weak or inconsistent responses. Vatinoxan attenuated α2-adrenoceptor agonist-induced responses, although the magnitude and nature of antagonism differed between species and experimental conditions. Noradrenaline-induced contraction was also attenuated by vatinoxan, whereas methoxamine produced little or no contraction and prazosin had minimal effects on noradrenaline responses. These findings support a predominant functional contribution of α2-adrenoceptors to vascular contraction in the chelonian systemic arteries studied, with comparatively little detectable contribution from α1-adrenoceptors. This adrenergic organization differs from the α1-dominant vascular regulation typical of mammals and identifies chelonian arteries as a useful comparative model for α2-adrenoceptor-mediated vascular control. The findings also provide a mechanistic basis for the peripheral vascular component of the cardiovascular response to α2-adrenoceptor agonist sedation in chelonians.NEW & NOTEWORTHY Chelonian systemic arteries exhibit predominantly α2-adrenoceptor-mediated contraction, with minimal functional contribution from α1-adrenoceptors, contrasting with mammalian vascular regulation. Medetomidine and detomidine induce robust vasoconstriction that is abolished by the peripherally acting α2-adrenoceptor antagonist vatinoxan. These findings identify a distinct adrenergic hierarchy in chelonian vasculature, provide a mechanistic basis for the cardiovascular effects of α2-agonist sedation, and establish chelonians as a comparative model of α2-adrenoceptor-mediated vascular regulation.