PubMed · 15865716
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Anthony Schaeffer, Jeffrey Stern, Thomas Jang. 2004. Chronic prostatitis.. https://pubmed.ncbi.nlm.nih.gov/15865716/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: We used a real-time reverse transcriptase polymerase chain reaction (RT-PCR) method for quantification of each alpha(1)-adrenoceptor (alpha(1)-AR) subtype expression level, and examined whether age and prostate volume influence human prostate alpha(1)-AR subtype expression. METHODS: Enrolled in our study were 75 men with lower urinary tract symptoms (LUTS) secondary to untreated benign prostatic hyperplasia (BPH). Real-time RT-PCR was performed using prostate biopsy specimens to quantify the expression level of each alpha(1)-AR subtype. RESULTS: The median expression level (interquartile range) was 1.24 (0.66-2.32), 0.16 (0.10-0.33), and 1.11 (0.75-2.27) x 1,000 copies/beta-actin for alpha(1a)-, alpha(1b)-, and alpha(1d)-AR mRNA, respectively. The expression levels differed with the individual. The expression levels of alpha(1a)-AR, alpha(1d)-AR, and total alpha(1)-AR mRNA showed a significant positive correlation with patient age, but did not correlate with prostate volume. CONCLUSION: The difference in the expression of the alpha(1)-AR subtype with the patient may be the cause of the difference in the effectiveness of several subtype-selective alpha(1)-AR antagonists from patient to patient. The increase of alpha(1)-AR mRNA expression level with age could be an important factor in the pathogenesis of clinically significant BPH.
Treatment with alpha(1)-adrenergic receptor blockers improves lower urinary tract symptoms (LUTS) secondary to benign prostatic hyperplasia. This study was conducted to test the hypothesis that induction of apoptosis in prostate tissue could be a mechanism underlying the observed clinical benefit. This placebo-controlled, double-blind, randomized trial enrolled 536 men with LUTS who were treated with alfuzosin (10 or 15 mg) once daily or placebo for 3 months. Total prostate and transition zone volume was measured by standardized transrectal ultrasound measurements at baseline and 3 months. Total prostate volume increased by 0.4 ml from baseline in placebo patients but decreased by -0.25 ml in the combined alfuzosin groups. Percentage change was not statistically significantly different between the placebo and alfuzosin groups. Changes in transition zone volumes from baseline were similar in both treatment arms; percentage change was not statistically significantly different between the placebo and alfuzosin groups. Volume changes did not correlate with prostate volumes at baseline. Overall, neither total prostate nor transition zone volume increased or decreased systematically within the 3-month treatment period. If alfuzosin-induced apoptosis in prostate tissue, it was not evident by a measurable change in prostate volume after 3 months' treatment. Further analysis at 1 and 2 years will determine the effect of longer-term treatment.
BACKGROUND: Prenatal cocaine exposure produces attentional deficits which to persist through early childhood. Given the role of norepinephrine (NE) in attentional processes, we examined the forebrain NE systems from prenatal cocaine exposed rats. Cocaine was administered during pregnancy via the clinically relevant intravenous route of administration. Specifically, we measured alpha2-adrenergic receptor (alpha2-AR) density in adolescent (35-days-old) rats, using [3H]RX821002 (5 nM). RESULTS: Sex-specific alterations of alpha2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of alpha2-AR in parietal cortex. CONCLUSION: These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.