Fructose feeding induces a moderate increase in blood pressure, insulin resistance, and hyperinsulinemia. This study investigated the role of α(1B)-adrenoceptor subtype in the control of renal hemodynamic responses to exogenously administered angiotensin II (Ang II) and a set of adrenergic agonists in a model of high fructose-fed rats.
Sprague-Dawley rats were fed for 8 weeks with 20% fructose in drinking water (FFR). The renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II in the presence and absence of chloroethylclonidine (CEC) (α(1B)-adrenoceptor antagonist) was determined. Data, mean ± SEM or SD were subjected to ANOVA with significance at p < .05.
FFR showed significant increase in the systolic blood pressure, plasma glucose, and insulin levels when compared to control. FFR expressed reduced renal cortical vascular sensitivity to NA, PE, ME, and Ang II. Furthermore, renal cortical vasoconstriction response to NA, PE, ME, and Ang II was blunted in the presence of CEC in control. While in FFR, renal cortical vasoconstriction to NA, PE, and ME was enhanced by CEC. Renal cortical vasoconstriction to Ang II in FFR was reduced in the presence of CEC.
In the presence of a hyperinsulinemic state resulting from chronic and high fructose feeding, an attenuated AT(1) and α(1)-adrenoceptors response to Ang II and adrenergic stimuli respectively, is expected. In addition, α(1B)-adrenoceptor is the functional subtype that mediates renal cortical vasoconstriction in control rat, while high fructose feeding did influence the functionality of α(1B)-adrenoceptor in mediating the renal cortical hemodynamic changes.