Modulation of Alpha 1 Adrenergic Receptors on Urinary Bladder in Rat Spinal Cord Injury Model.
- Author:
Gilho LEE
1
;
Heeyoon PARK
;
Hong Suk PARK
;
Jeong Gu LEE
Author Information
1. Department of Urology, Dankook University College of Medicine, Cheonan, Korea. prostate@ymail.com
- Publication Type:Original Article
- Keywords:
Spinal cord injuries;
Urinary bladder;
Alpha adrenergic receptors
- MeSH:
Animals;
DNA, Complementary;
Female;
Humans;
Oxidoreductases;
Plasmids;
Rats;
Rats, Sprague-Dawley;
Real-Time Polymerase Chain Reaction;
Receptors, Adrenergic;
Receptors, Adrenergic, alpha;
Receptors, Adrenergic, alpha-1;
RNA;
RNA, Messenger;
Spinal Cord;
Spinal Cord Injuries;
Urinary Bladder;
Urinary Bladder, Neurogenic
- From:International Neurourology Journal
2012;16(2):62-68
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Whereas many studies have focused on the vesical changes of the alpha1 adrenergic receptor (AR) subtypes in partial outlet obstruction, few studies have addressed the modulation of the alpha1 AR subtypes after spinal cord injury (SCI). Therefore, we studied the modulation of the alpha1 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 alpha1 ARs (alpha1a, alpha1b, and alpha1d) 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 alpha1 ARs was lower in the SCI group than in the control animals. The alpha1a, alpha1b, and alpha1d mRNA expression in the controls was 81.7%, 3.3%, and 15.1%, respectively, whereas the alpha1a, alpha1b, and alpha1d mRNA expression in the SCI group was 33.5%, 5.2%, and 60.9%, respectively. CONCLUSIONS: SCI moderates the alpha1 AR mRNA subtypes in the urinary bladder. The relatively increased alpha1d or decreased alpha1a AR mRNA expression may be a therapeutic candidate for controlling the symptoms of neurogenic bladder after SCI.
