Influence of high-fructose feeding on functional α1-adrenoceptor subtypes in the rat kidney

This study investigated whether the α1-adrenoceptor responsiveness of the renal vasculature was altered in a metabolic syndrome state due to high-fructose feeding. Male Sprague-Dawley rats were fed for 8 weeks with 20% fructose in the drinking water (FFR). They were pentobarbitone anaesthetized and the reductions in renal cortical blood flow to intrarenal administration of noradrenaline, phenylephrine, methoxamine and angiotensin II (Ang II) were determined before and after 5-methylurapidil, chloroethylclonidine (CEC) or BMY 7378. Data, mean±SEM were subjected to ANOVA with significance at P<0.05. FFR had higher systolic blood pressure, plasma glucose and insulin level as compared to control (FFR vs. control, 123±2 vs. 107±1 mmHg, 6.8±0.3 vs. 5±0.3 mmol/L and 2.8±0.2 vs. 1.9±0.2 ng/ml) respectively. FFR expressed reduced (P<0.05) renal vascular responses to noradrenaline, phenylephrine, methoxamine and Ang II by 36%, 26%, 41% and 56% respectively. The response to Ang II was attenuated by 5-methylurapidil, CEC and BMY 7378 in the FFR and control, while the adrenergic responses were blunted by 5-methylurapidil and enhanced by CEC and BMY 7378 in the FFR. These findings suggest that α1A-adrenoceptor is the functional subtype that mediates renal vasoconstriction response in FFR.