Key result
Prazosin and 5-methyl-urapidil completely abolish prostate tension, localizing alpha-1A adrenoceptors to synaptic regions.
Why the study?
The functional roles and subtype characterization of alpha 1-adrenoceptors in human prostate tension response to electrical field stimulation were not fully understood.
Answers are grounded in this paper and cite their sources.
The study demonstrates that putative alpha 1A-adrenoceptors primarily mediate the contractile response to electrical field stimulation in the human prostate.
The effects of various alpha 1-adrenoceptor antagonists and nifedipine on tension responses of human prostate to electrical field stimulation were evaluated in this study. 2. Prazosin (3 x 10(-10) to 10(-8) M) and 5-methyl-urapidil (10(-9) to 3 x 10(-8) M) blocked concentration-dependently the tension responses to electrical field stimulation and completely abolished them in the maximal concentrations (10(-8) M and 3 x 10(-8) M, respectively); in contrast, chloroethylclonidine (CEC), in the maximal concentration of 100 microM, blocked these effects by only 50%. 3. The contractile responses of rat vas deferens and spleen to exogenously-applied alpha 1-adrenoceptor agonists were competitively inhibited by prazosin and 5-methyl-urapidil; in addition, the pA2 values were calculated and the relative potencies with reference to prazosin were obtained. The relative potency of 5-methyl-urapidil in human prostate (0.105) was close to that in rat vas deferens (0.257), which contains primarily putative alpha 1A-adrenoceptors. However, it was much more than that in rat spleen (0.011), which contains primarily putative alpha 1B-adrenoceptors. 4. Nifedipine (10(-8) to 10(-6) M) inhibited concentration-dependently the contractile responses to electrical field stimulation in human prostate; in addition, the inhibition percentages were similar to those to exogenously-applied noradrenaline in rat vas deferens. In contrast, CEC (10 microM), which almost flattened the concentration-response curve of the rat spleen to phenylephrine, only partially inhibited (by 33.1%) the nerve-mediated contraction of human prostate. 5. The involvement of prejunctional alpha 2-adrenoceptors situated on the sympathetic nerve terminals of human prostate was also examined. Clonidine (3 x 10-9 to 3 x 10- M) blocked concentration-dependently the contractile response to electrical field stimulation of human prostate and this inhibitory effect was reversed by yohimbine (10-7 M). Additionally, the inhibitory effect of CEC (3 x 10-6 to 3 x 10-4 M)to the nerve-mediated contraction was also partially reversed by yohimbine (10-7 M).6. It is suggested that the putative czA-adrenoceptors in human prostate may be functionally confined to the synaptic region whereas only minor populations of the putative alpha 1B- and/or alpha 1c-adrenoceptors exist in this region.
No takes yet. Share an insight, caveat, or question.
Guh et al. (1995) studied this question. Alpha 1-adrenoceptor antagonists (prazosin, 5-methyl-urapidil, chloroethylclonidine) and nifedipine was evaluated on Tension responses to electrical field stimulation. Prazosin and 5-methyl-urapidil completely abolished tension responses to electrical field stimulation in human prostate, suggesting alpha-1A adrenoceptors are functionally confined to the synaptic region.
Synapse has enriched 10 related papers. Consider them for comparative context: