The present study hypothesized that chronic administration of candesartan will not only improve the sensitivity of alpha-adrenergic receptors to adrenergic agonists but also modulate the expression of angiotensin receptors (AT1a) and sodium chloride cotransporter (NCC) mRNAs. Animals were divided into four groups WKY control; WKY received candesartan (WKY-CST, 10 mg/kg), SHR control, and SHR received candesartan (SHR-CST). Plasma, urine samples, and mean arterial pressure (MAP) were taken on days 0, 21, and 28. Acute studies determined the renal vasoconstrictor actions of Ang II, noradrenaline (NA), phenylephrine (PE), and methoxamine (ME). The overall mean drops in renal cortical blood perfusion (RCBP) to NA, PE, ME, and Ang II were significantly increased in WKY-CST and SHR-CST when compared to the respective control. Expression of AT1a mRNA in the kidney of WKY-CST and SHR-CST were increased 11 folds and 8 folds respectively when compared to internal control (β-actin). Expression of NCC MRNA in the kidney of WKY-CST and SHR-CST were 10 folds and 6 folds respectively when compared to internal control. Candesartan restores the functional responsiveness of alpha-adrenergic receptors in normal and spontaneously hypertensive rats by alleviating mean arterial pressure, enhancing renal cortical blood perfusion, and increasing the functional capabilities of the kidney by modulating renal tubular and glomerular functions. Secondly, chronic administrations of candesartan in SHR regulated the expression of AT1a mRNA and NCC mRNA in SHR rat kidneys when compared to SHR control rats.