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.