alpha(1)-adrenoceptor modulation of spontaneous electrical waveforms in the guinea-pig prostate.

The aim of this study was to investigate the effects of phenylephrine on the spontaneous slow wave and pacemaker activity in the guinea-pig prostate. Membrane potential recordings were made using intracellular microelectrodes. Guinea-pig prostatic cells either displayed 'slow wave' activity or 'pacemaker' potentials. In the presence of nifedipine, none of the parameters measured were significantly different between both waveforms. Phenylephrine (1 microM) or histamine (5 microM) increased the frequency of slow waves and pacemaker potentials in the absence or presence of nifedipine (1 microM). In the presence of nifedipine (1 microM), the addition of either cyclopiazonic acid (CPA, 10 microM) or carbonyl cyanide 3-chlorophenylhydrazone (CCCP, 1-10 microM) caused an initial transient increase in frequency of the spontaneous electrical activity that was associated with a membrane depolarisation of 3-7 mV before abolishing activity. Following the cessation of electrical activity, phenylephrine (1 microM) was unable to restore the spontaneous electrical events. Although niflumic acid (10-100 microM) (in the presence of 1 microM nifedipine) similarly abolished all activity, electrical activity was promptly initiated upon the addition of phenylephrine (1 microM). These results demonstrate that in the presence of nifedipine, there are no differences between the slow waves and pacemaker potentials suggesting that both activities arise from cells that are well coupled. Both phenylephrine and histamine increased the frequency of pacemaker activity which is likely to; at least, partly explain the increase in slow wave discharge also evoked by these agents. In the presence of nifedipine, the effects observed upon alpha(1)-adrenoceptor activation were dependent on Ca(2+) cycling by both the intracellular Ca(2+) stores and mitochondria.