Cystometries were performed in normal rats and in rats with bladder hypertrophy due to infravesical outflow obstruction. Investigations were performed in the presence and absence of anesthesia. pentobarbital anesthesia depressed spontaneous contractile activity in the bladder and the micturition reflex, thereby making measurements of other variables, such as bladder capacity and residual volume, impossible. In conscious animals infravesical outflow obstruction led to development of increased bladder capacity, marked residual volume, and unstable detrusor contractions. The model seems to be well suited for further evaluation of the mechanisms involved in the development of detrusor instability and the responses to pharmacological treatment.
SUMMARY1. The effects of continuous preganglionic stimulation of the chorda tympani at 2 Hz for 10 min were compared with those of stimulation at 20 Hz in 1 see bursts at 10 see intervals for the same period in cats treated with atropine (0-5 mg/kg). Both the fall in mean submaxillary vascular resistance (s.v.r.) and the rise in mean vasoactive intestinal peptide (VIP) output from the gland were increased significantly (P < 0-01; P < 0 02) when the same total number of impulses were delivered in the form of bursts at the higher frequency.2. Both responses were also consistently increased by stimulating the postganglionic innervation in bursts in atropinized cats, or by stimulating the preganglionic innervation in bursts in the absence of atropine.3. The effects of stimulation of the chorda tympani in 1 see bursts at 10 see intervals for 2-3 min were investigated over the frequency range 2-160 Hz. The change in mean s.v.r. under these conditions was significantly reduced by administration of atropine at frequencies between 2 and 20 Hz, but not at higher frequencies. In atropinized cats, the fall in mean s.v.r. was linearly related to stimulus frequency (r = 0 993) over the range 2-60 Hz and a maximal response was obtained during stimulation at 80 Hz. In the same experiments the fall in mean s.v.r. was linearly related to log mean VIP output over the frequency range 20-160 Hz (r = 0 998).4. Closely similar changes in mean s.v.r occurred in response to both pre-and post-ganglionic stimulation at all frequencies tested between 2 and 160 Hz in atropinized cats when the stimuli were delivered in bursts. The changes in mean s.v.r. were not significantly affected by varying the duration of individual stimuli over the range 0-1-25-0 msec.5. The flow of submaxillary saliva was also linearly related to stimulus frequency over the range 2-40 Hz (r = 0 997) when the stimuli were delivered in bursts in the absence of atropine and secretion of saliva was maximal at 60 Hz.6. It is concluded that release of VIP from the submaxillary gland of the cat is optimal in response to stimulation of the chorda tympani at relatively high frequencies, when the impulses are delivered in bursts. Flow of saliva which is mediated by acetyl choline, may also be potentiated under the same conditions.
SUMMARY1. The haemodynamics of erection were elucidated in the anaesthetized dog by analysing in quantitative terms the changes of penile arterial inflow, venous outflow and tissue volume during graded pelvic nerve stimulation. The study also provides information on possible neurotransmitter mechanisms of the erectile response.2. Erection evoked by pelvic nerve stimulation appeared to result from two main circulatory events: first, there was a prompt dilatation of the penile 'resistance vessels', causing a greatly increased arterial inflow which in the early phase bypassed the cavernous bodies and, hence, increased venous outflow to the same extent. Secondly, the erectile response proper began after a distinct delay (,-20 s). This was apparently caused by sudden opening of low resistance 'shunt vessels' diverting part of the arterial inflow into the cavernous bodies, leading to rapid filling. During the filling phase arterial inflow greatly exceeded venous outflow, and returned to the venous outflow level again in the steady state of full erection. The initial dilator response seemed to ensure rapid erection by establishing a high pressure head from the arterial microvessels to the cavernous spaces.3. The threshold frequency for the penile vasodilator response to pelvic nerve stimulation was 1-2 Hz and was always higher for the erectile volume response, viz. 2-4 Hz. Maximal effects for both were obtained at 16 Hz, causing on the average a 25-fold increase in peak arterial inflow, a 17-fold increase in venous outflow and a 107 % increase in penile volume. 4. Muscarinic blockade by atropine caused no significant decrease in the blood flow response induced by pelvic nerve stimulation, but clearly curtailed the erectile response. This indicates that the dilatation of the penile 'resistance vessels' is mainly non-cholinergic in nature, whereas a cholinergic mechanism seems to contribute to the erectile volume response proper.5. Pelvic nerve stimulation caused a substantial output of vasoactive intestinal polypeptide (VIP) from the penis which was correlated in onset and duration to theThe experimental work was performed at the
This work reports the results of the first functional characterization of the alpha 1c-adrenoceptor subtype. The most functionally important alpha 1-adrenoceptor type in the human prostate appears to be the alpha 1c subtype. This finding may aid the development of prostate-selective adrenoceptor pharmacotherapy.
Normal rats as well as rats with bladder hypertrophy secondary to outflow obstruction were investigated cystometrically before and after administration of the potassium channel openers pinacidil or cromakalim one mg./kg. orally. In normal rats cromakalim decreased micturition pressure by 15 +/- 6%. A diminished micturition pressure was also seen after pinacidil (by 18 +/- 8%) but this did not achieve statistical significance. Further, no clear-cut effects on bladder capacity, residual volume, basal bladder pressure, threshold pressure, bladder compliance or on bladder wall tension were seen in this group of rats neither in the presence of pinacidil nor cromakalim. Rats with bladder hypertrophy exhibited a significant bladder instability during cystometrical investigations. The mean amplitude of the spontaneous bladder contraction exceeded 20 cm. H2O prior to micturition. Administration of pinacidil and cromakalin decreased the spontaneous contractions to 26 +/- 12% and 22 +/- 7%, respectively, of that seen in the absence of the drugs. Furthermore, pinacidil decreased micturition pressure by 61 +/- 12%. Also cromakalim decreased micturition pressure (by 27 +/- 13%) but this effect did not achieve statistical significance. After both pinacidil and cromakalim these rats tended to develop residual urine. In accordance with the results in normal rats pinacidil and cromakalim showed no effects on bladder capacity, basal bladder pressure, threshold pressure, bladder compliance or on bladder wall tension in rats with bladder hypertrophy. The findings of an almost complete disappearance of spontaneous bladder contractions in rats with bladder instability and a remaining voiding ability after administration of pinacidil or cromakalim suggest that potassium channel openers may be a therapeutic alternative in the treatment of bladder instability associated with outflow obstruction.
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