PubMed · 15999767
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Hiroshi Yamasaki, Hideyuki Sasaki, Machi Furuta. 2005. [Bladder dysfunction in diabetics].. https://pubmed.ncbi.nlm.nih.gov/15999767/
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The role of the alpha-adrenergic system in the control of cardiac preload (central venous blood pressure; P(ven)) and venous capacitance during exercise was investigated in rainbow trout (Oncorhynchus mykiss). In addition, the antihypotensive effect of the renin-angiotesin system (RAS) was investigated during exercise after alpha-adrenoceptor blockade. Fish were subjected to a 20-min exercise challenge at 0.66 body lengths s(-1) (BL s(-1)) while P(ven), dorsal aortic blood pressure (P(da)) and relative cardiac output (Q) was recorded continuously. Heart rate (f(H)), cardiac stroke volume (SV) and total systemic resistance (R(sys)) were derived from these variables. The mean circulatory filling pressure (MCFP) was measured at rest and at the end of the exercise challenge, to investigate potential exercise-mediated changes in venous capacitance. The protocol was repeated after alpha-adrenoceptor blockade with prazosin (1 mg kg(-1)M(b)) and again after additional blockade of angiotensin converting enzyme (ACE) with enalapril (1 mg kg(-1)M(b)). In untreated fish, exercise was associated with a rapid (within approx. 1-2 min) and sustained increase in Q and P(ven) associated with a significant increase in MCFP (0.17+/-0.02 kPa at rest to 0.27+/-0.02 kPa at the end of exercise). Prazosin treatment did not block the exercise-mediated increase in MCFP (0.25+/-0.04 kPa to 0.33+/-0.04 kPa at the end of exercise), but delayed the other cardiovascular responses to swimming such that Q and P(ven) did not increase significantly until around 10-13 min of exercise, suggesting that an endogenous humoral control mechanism had been activated. Subsequent enalapril treatment revealed that these delayed responses were in fact due to activation of the RAS, because resting P(da) and R(sys) were decreased further and essentially all cardiovascular changes during exercise were abolished. This study shows that the alpha-adrenergic system normally plays an important role in the control of venous function during exercise in rainbow trout. It is also the first study to suggest that the RAS may be an important modulator of venous pressure and capacitance in fish.
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.