Adult rats exposed to maternal separation (MatSep) are normotensive but display lower glomerular filtration rate and increased renal neuroadrenergic drive. The aim of this study was to determine the renal alpha-adrenergic receptor density and the renal vascular responsiveness to adrenergic stimulation in male rats exposed to MatSep. In addition, baroreflex sensitivity was assessed to determine a component of neural control of the vasculature. Using tissue collected from 4-month-old MatSep and control rats, alpha 1-adrenergic receptors (α1-ARs) were measured in renal cortex and isolated renal vasculature using receptor binding assay, and the α-AR subtype gene expression was determined by RT-PCR. Renal cortical α1-AR density was similar between MatSep and control tissues (Bmax=44±1 vs. 42±2 fmol/mg protein, respectively); however, MatSep reduced α1-AR density in renal vasculature (Bmax=47±4 vs. 62±4 fmol/mg protein, p<0.05, respectively). In a separate group of rats, the pressor, bradycardic and renal vascular constrictor responses to acute norepinephrine injection (NE, 0.03-0.25 μg/μl) were determined in anesthetized rats. MatSep rats showed attenuated NE-induced renal vasoconstriction compared to control rats (p <0.05). A third group of rats was infused at steady state with the α1 agonist phenylephrine (PE, 10 μg/min, i.v.) and vasodilator sodium nitroprusside (SNP, 5 μg/min, i.v.). The difference between the HR/MAP slopes was indicative of reduced baroreflex sensitivity in MatSep vs. control rats (-0.45±0.04 vs. -0.95±0.07 bpm/mmHg, p<0.05). These data support the notion that reduced α-adrenergic receptor expression and function in the renal vasculature could develop secondary to MatSep-induced overactivation of the renal neuroadrenergic tone.