Modulation of Alpha 1 Adrenergic Receptors on Urinary Bladder in Rat Spinal Cord Injury Model

Abstract

Purpose: Whereas many studies have focused on the vesical changes of the alpha 1 adrenergic receptor (AR) subtypes in partial outlet obstruction, few studies have addressed the modulation of the alpha 1 AR subtypes after spinal cord injury (SCI). Therefore, we studied the modulation of the alpha 1 ARs in urinary bladder in a rat SCI model. Methods: Four weeks after a SCI, the whole vesical bodies from eight female Sprague-Dawley rats and from eight controls were harvested. The total RNA was extracted from the samples and was used to prepare cDNA. We developed standard plasmid constructs of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and three alpha 1 ARs (alpha 1a, alpha 1b, and alpha 1d) to convert the cycle threshold (Ct) values from real-time polymerase chain reaction (RT-PCR) into subtype mRNA concentrations. The detected Ct values of 16 samples from RT-PCR were interpolated into the standard plasmid curves. Results: All serially diluted standard samples showed very good linearity. The mRNA expression of GAPDH was higher in the SCI group, whereas the mRNA expression of all alpha 1 ARs was lower in the SCI group than in the control animals. The alpha 1a, alpha 1b, and alpha 1d mRNA expression in the controls was 81.7%, 3.3%, and 15.1%, respectively, whereas the alpha 1a, alpha 1b, and alpha 1d mRNA expression in the SCI group was 33.5%, 5.2%, and 60.9%, respectively. Conclusions: SCI moderates the alpha 1 AR mRNA subtypes in the urinary bladder. The relatively increased alpha 1d or decreased alpha 1a AR mRNA expression may be a therapeutic candidate for controlling the symptoms of neurogenic bladder after SCI.