Hypogastric Nerve Stimulation Research Articles

Neural regulation of the vas deferens in the rat: an electrophysiological analysis.

Electrophysiological analysis of the neural control of the vas deferens was performed in urethan-anesthetized rats. Intraluminal distension (0.2 ml/min) or electrical stimulation of hypogastric (threshold 1-5 V, 20 Hz) and pelvic nerves (2-5 V, 20 Hz) produced contractions of the vas deferens. Distension-evoked contractile activity was not abolished by nicotinic ganglionic blockade or ipsilateral hypogastric and pelvic nerve transection. Contractions following hypogastric nerve stimulation were abolished by prazosin, while pelvic nerve-evoked responses were partially blocked by atropine. Hypogastric nerve, pelvic nerve, and sympathetic chain stimulation evoked volleys with latencies of 10-30 ms in vasal nerves. Crude estimates for conduction velocities for these responses (less than 0.5 m/s) corresponded to activation of unmyelinated C-fibers. Stimulation of the dorsal nerve of the penis (DNP) (10-16 V, 10-40 Hz) or administration of 5-methoxy-N,N-dimethyltryptamine, both of which produce seminal emission, elicited reflex discharges in nerves to the vas deferens. Hypogastric nerve but not pelvic nerve transection abolished both spontaneous and evoked (105- to 380-ms latency) reflex activity. These experiments provide insight into the organization of afferents in the DNP and efferents conveyed by autonomic pathways that regulate male reproduction.

An electromyographic study of the feline urethral rhabdosphincter in the normal state and after sacral rhizotomy. Part 2. Responses of the rhabdosphincter to hypogastric nerve stimulation

To investigate functional aspect of sympathetic innervation of the urethral rhabdosphincter, responses of the male feline rhabdosphincter to hypogastric nerve (HGN) stimulation were examined by means of electromyography using fine electrodes. Experiments were performed on 28 normal (N group) and 13 rhizotomized cats under chloralose anesthesia, the latter being further divided into two groups: 4 cats of 1-3 weeks (SR group) and 9 cats of 10-24 weeks (LR groups) after complete sacral rhizotomy. HGN stimulation (1 Hz, 0.3 ms pulse duration, 2-30 V) elicited responses of the rhabdosphincter in N and LR groups. In N group, HGN stimulation still elicited responses of the rhabdosphincter even after pudendal nerve was transected in advance, indicating that these evoked potentials were independent of somatic nerve inflow. The threshold stimuli and latencies of the evoked responses in N group (3.0 +/- 0.2 V, 81.7 +/- 5.7 ms, respectively) were not significantly different from those in LR group (2.9 +/- 0.3 V, 71.5 +/- 10.5 ms), but the amplitudes of the evoked responses were significantly larger in LR group than in N group (110 +/- 12 vs 18 +/- 2 microV, p less than 0.001). These evoked responses of the rhabdosphincter were resistive to prazosin (0.2 mg/kg) and atropine (0.5 mg/kg), but were abolished by hexamethonium (2 mg/min, 10-25 mg) and pancuronium (0.1-0.3 mg/kg) in both groups. In N group, repetitive stimulation (10-20 Hz) of HGN increased activities of the rhabdosphincter when the bladder was empty, but not when the bladder was full enough to trigger the vesicourethral relaxation reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin E 2 selectively affects purinergic transmission in guinea pig vas deferens

The effect of prostaglandin E 2 (PGE 2) on the contractile response of the guinea pig vas deferens was examined. Postganglionic hypogastric nerve stimulation for 7 sec at 20 Hz induced a biphasic contractile response, consisting of fast phasic and delayed tonic components. Prostaglandin E 2 delayed the onset and increased the maximum contractile responses. Stimulation in the presence of prazosin induced only a fast phasic contraction. Treatment with PGE 2, in the presence of prazosin, delayed the onset of this response and increased its maximum. The delayed contraction, observed on stimulation in the presence of α,β-methylene adenosine triphosphate (ATP), was enhanced moderately and concentration-dependently by PGE 2. Short-term stimulation with 5 pulses induced a small fast phasic contraction. This contraction, which could be desensitized by α,β-methylene ATP, was inhibited by PGE 2 but not by prazosin. Prostaglandin E 2 significantly enhanced the transient phasic contraction, induced by addition of exogenous ATP to the organ bath and had a similar but somewhat smaller effect on the tonic contraction induced by the addition of exogenous norepinephrine (NE). These findings suggest that PGE 2 selectively delayed neurotransmission, mediated by ATP and enhanced contractions of the smooth muscle of guinea pig vas deferens, elicited by ATP or NE.

Sympathetic innervation of the male feline urethral rhabdosphincter

Sympathetic innervation of the male feline urethral rhabdosphincter was investigated by means of electromyography (EMG). Hypogastric nerve stimulation elicited responses in the rhabdosphincter, the latencies and amplitudes ranged from 40 to 107 ms and 6 to 40 μV, respectively. These hypogastric nerve-evoked responses in the rhabdosphincter were not affected by whether the urinary bladder was empty or full. The results suggest that hypogastric nerve-evoked responses in the rhabdosphincter are not dependent on somatic nerve, but are produced through a rather direct effect of sympathetic nerve on the rhabdosphincter.

交感神経刺激に対するネコ尿道の反応

The responses of the urethra to hypogastric nerve (HGN) and lumbosacral sympathetic chain (SC) stimulation were observed in 25 chloralose-anesthetized cats. Urethral perfusion pressure was monitored as an index of functional urethral responses. SC was stimulated at four points from L4 to S1. Urethral constrictive response induced by HGN stimulation (delta P:HGN) was significantly larger in male cats than in female cats. But there was no difference between male and female cats in urethral constrictive response induced by SC stimulation (delta P:SC). delta P:HGN was significantly larger than delta P:SC in both sexes, and the ratio of delta P:HGN to delta P:SC (L7-S1) was 2.7 to 1 in male cats and 1.7 to 1 in female cats. delta P:HGN was blocked by the alpha-adrenergic antagonist phentolamine (1-2 mg/kg) and reduced about 50% by autonomic ganglion blockade with hexamethonium bromide (2 mg/min, 25-50 mg). delta P:SC was blocked by both phenotolamine and hexamethonium bromide. In order to examine the pathways of projections of sympathetic fibers from the sacral SC to the urethra, HGN, pelvic nerve and pudendal nerve were transected serially. delta P:SC (L7-S1) was decreased 0%, 12% and 50% by transection of HGN, pelvic nerve and pudendal nerve, respectively. After severance of these three nerves, delta P:SC (L7-S1) was reduced 62%, but not abolished. These data suggest: 1) The effect of HGN to the feline urethra is more prominent than that of SC in both sexes and significantly larger response was noted in male cats with HGN stimulation but not with SC.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Hypogastric Nerve and Sympathetic Chain Stimulation on the Pelvic Nerve Induced Penile Erection in the Dog

The effects of electrical stimulation of hypogastric nerve and sympathetic chain on 'electroerection' (penile erection induced by electrical stimulation of the pelvic nerve) were studied in dogs to clarify the physiological roles that these neural inputs may play in producing and/or maintaining penile erection. As an objective parameter of hemodynamics of the penile circulation, the pressure in the corpus cavernosum of the penis was measured. Hypogastric nerve electrostimulation was performed in 24 dogs who had received pelvic nerve stimulation and, therefore, had 'electroerection'. Ten dogs responded to this procedure with an augmentation of 'electroerection', 10 with an attenuation of 'electroerection', and 4 with no appreciable changes. 4 out of the 10 animals who exhibited an attenuation response were then given an alpha 1-adrenergic blocker (prazosin hydrochloride) prior to the electrical stimulation to evaluate the specificity of the effects of the hypogastric nerve stimulation. In 3 of the 4 dogs the attenuation effect was abolished by this treatment and instead an augmentation effect became evident. Sympathetic chain electrostimulation was performed in 6 dogs with 'electroerection'. When applied to the L4-5 interganglionic segment, it produced a biphasic response which consisted of an initial increase followed by a decrease of the intracorporeal pressure. In contrast, stimulation of the L2-3 interganglionic segment produced a monophasic response consisting of only augmentation of the intracorporeal pressure. These data suggested that there might be two groups of fibers in the hypogastric nerve and sympathetic chain which are functioning antagonistically, and that the anti-erectile neural inputs are mediated primarily by the alpha 1-adrenergic system. To examine the sites of penile vasculature where the innervating hypogastric nerve exerts its effects, electrical pelvic/hypogastric nerve stimulations were performed in dogs in whom the inflow blood circulation to the corpora cavernosa was disrupted by arterial ligation and replaced by a constant saline infusion. It appears that the stimulatory input via the hypogastric nerve caused an increased blood flow into the cavernous space due to vasodilation of the inflow blood vessels, and the inhibitory effect occurred mainly due to relaxation of the draining blood vessels with a resultant increase of the blood outflow from the cavernous space.

Urethral Function after Chronic Cauda Equina Lesion in Cats. II. The Role of Autonomically-Innervated Smooth and Striated Muscle in Distal Sphincter Dysfunction

We investigated the possibility that distal sphincter dysfunction after chronic sacral rhizotomy in the cat might be due to altered sympathetic influences on smooth and striated muscle. Three months after rhizotomy, sympathetic influences on basal perfusion pressure in the distal sphincteric urethra were significantly decreased. A prazosin-sensitive component of basal perfusion pressure remained after section of all extrinsic urethral innervation in both control and chronic cats. Local intra-arterial 6-hydroxydopamine also abolished this component. After rhizotomy, noradrenaline content in the distal sphincteric urethra was significantly increased but there was no evidence of a change in sensitivity to sympathetic stimulation. A novel prazosin- and atropine-resistant component of the response to hypogastric nerve stimulation was seen in the rhabdosphincteric urethra of chronic cats. This component was abolished by atracurium or hexamethonium. It was significantly greater in cats with S1-3 as compared to S2-3 lesions and was never seen in control cats. It is concluded that autonomic activation of the rhabdosphincter could be a factor in distal sphincter obstruction. (J. Urol., 144: 1029–1035, 1990)

Urinary bladder and urethral responses to pelvic and hypogastric nerve stimulation and their relation to vasoactive intestinal polypeptide in the anaesthetized dog

The effects on the urinary bladder and urethra of pelvic and hypogastric nerve stimulation and their relation to vasoactive intestinal polypeptides (VIP) were investigated in the anaesthetized dog. Both pelvic and hypogastric nerve stimulation elicited a twofold increase in urinary bladder blood flow and a clear-cut increase in bladder venous effluent VIP concentration. Hypogastric nerve stimulation induced an initial, partly alpha-adrenergic and partly non-adrenergic, non-cholinergic, contraction of the urinary bladder followed by a relaxation. The urethra response was a maintained alpha-adrenergic contraction. Pelvic nerve stimulation elicited a bladder contraction with an initial non-cholinergic peak, whereafter the bladder pressure was maintained at a lower level, an effect which was mainly cholinergic in origin. The urethral response was an initial non-adrenergic, non-cholinergic contraction followed by a maintained cholinergic contractile response. Afferent pelvic nerve stimulation led to an efferent activity that seemed to be a combination of activity in pelvic and hypogastric pathways to the urinary bladder and the urethra. VIP (10 nmol) injected i.v. induced a relaxation of the urinary bladder and the urethra, together with a fall in systemic blood pressure. However, despite high plasma concentrations, no vasodilation was elicited in the urinary bladder. Thus, the main target for the VIP release during pelvic and hypogastric nerve stimulation is probably not the bladder vasculature, but instead perhaps the bladder smooth muscle proper.

Sympathetic modulation of cholinergic transmission in cat vesical ganglia is mediated by alpha 1- and alpha 2-adrenoceptors

Modulation of transmission in cat vesical ganglia by exogenous catecholamines or short periods of hypogastric nerve stimulation (HGS) was examined in vivo. HGS (30 Hz, 30 V, 10- to 20-s train) initially caused inhibition of ganglionic transmission, followed by a period of facilitation. The inhibition could be evoked by lower stimulus intensities than the facilitation. The biphasic effect was mimicked by norepinephrine (2-10 micrograms) injected into the inferior mesenteric artery, whereas phenylephrine (5-10 micrograms) usually caused only facilitation. The administration of specific adrenoceptor antagonists showed that the inhibitory responses were mediated by alpha 2-receptors and the facilitatory responses by alpha 1-receptors. The effects of HGS and norepinephrine were also tested on pelvic nerve-evoked bladder contractions. Both caused a brief reduction in contraction amplitude which, for the HGS effect, was mediated mainly by alpha 2-receptors. Noradrenergic inhibition of bladder contractions was mediated by both alpha 2- and beta-adrenoceptors. These studies have shown that sympathetic modulation of ganglionic transmission in the bladder can be either inhibitory or facilitatory, each mediated by a specific receptor type. These two actions may be important during different stages of bladder storage or voiding.

Penile erection in the rat: Stimulation of the hypogastric nerve elicits increases in penile pressure after chronic interruption of the sacral parasympathetic outflow

Penile erection, a vascular event mediated by the autonomic nervous system, is often adversely affected by injury to the spinal cord. To further characterize the laboratory rat as an animal model of penile erection and to investigate erectile responses following neural injury, the present study has examined pressor penile responses in intact rats and in animals deprived of sacral parasympathetic outflow. Increases in penile pressure result from graded stimulation of postganglionic parasympathetic fibers. The vasodilator response is insensitive to blockade with atropine, a cholinergic antagonist. Penile tumescence also results from stimulation of the pelvic nerve, but not the hypogastric nerve. However, beginning 3 days after unilateral interruption of the pelvic nerve, stimulation of the ipsilateral hypogastric nerve results in an increase in penile pressure. This novel response, which is blocked by a ganglionic antagonist, is maximally developed at 1 week post-lesion, is stable for at least 3 months and remains confined to the side of the lesion. These results suggest that the rat, although relatively small, can be used to obtain quantitative data on penile erection. Moreover, the model may lend itself to an analysis of the mechanisms of altered control of visceral tissues following injury to the nervous system.

Functional evaluation of sympathetically mediated responses in in vivo lower urinary tract of dogs

An in vivo procedure for evaluating local effects of α-adrenoceptor stimuli on the lower urinary tract was developed in anesthetized dogs. Electrical stimulation of hypogastric nerve at varied frequencies (1, 2, and 4 Hz) and intraarterial (i.a.) administration of an α 1-adrenoceptor agonist, phenylephrine (0.3, 1, and 3 μg) to the urethra and bladder through the cannulated right external iliac artery caused reproducible frequency- or dose-related increases in intraurethral pressure (IUP). Intrabladder pressure (IBP) was increased by the nerve stimulation but not by i.a. phenylephrine. Acetylcholine (10 μg) given i.a. elicited increases in both IUP and IBP. Prazosin (0.1, 1, and 10 μg kg , i.v.) dose-dependently suppressed the urethral contractile responses to the nerve stimulation and i.a. phenylephrine, but it failed to affect the bladder contraction evoked by the nerve stimulation. The results suggest that the urethral contractile responses to hypogastric nerve stimulation as well as i.a. phenylephrine were mediated via α 1-adrenoceptors, whereas the IBP increasing effect of hypogastric nerve stimulation was not mediated via α 1-adrenoceptors.

In vivo experiments for the evaluation of α 1-adrenoceptor antagonistic effects of SGB-1534 on canine urethra

The α 1-adrenoceptor blocking effects of SGB-1534 on the urethral smooth muscle were compared in in vivo lower urinary tract preparations of anesthetized dogs, with the effects of other α 1-adrenoceptor antagonists, Prazosin and bunazosin. Hypogastric nerve stimulation and selective administration of phenylephrine to the urethra and bladder through the cannulated right external iliac artery (i.a.) elicited reproducible frequency- and dose-dependent increases in intra-urethral pressure. Intra-bladder pressure was increased by the stimulation but not by i.a. phenylephrine. SGB-1534, prazosin or bunazosin (0.1–10 μg/kg i.v.) dose dependently suppressed the urethral contraction evoked by the nerve stimulation and i.a. phenylephrine but did not influence the bladder contraction elicited by nerve stimulation. The α 1-adrenoceptor blocking potency of SGB-1534 was approximately 2.3 and 8.1 times greater than that of prazosin and bunazosin, respectively. The results indicate that α 1-adrenoceptors may mediate mainly the urethral contraction induced by hypogastric nerve stimulation and i.a. phenylephrine, and that SGB-1534 was more potent α 1-adrenoceptor blocking activity than prazosin and bunazosin in the canine urethra.

Neurophysiological aspects of penile erection: the role of the sympathetic nervous system.

Recent studies have revealed that the initiation, maintenance and rigidity of penile erection are under parasympathetic and somatotopic control. The mechanism of penile detumescence is still under debate. Single and combined cavernous and hypogastric nerve stimulation was used to study the influence of the sympathetic nervous system on penile erection and to identify the mechanism of penile detumescence. Penile arterial flow and intracorporeal pressure recordings during various stimulation patterns indicated that erection induced by stimulation of the cavernous nerve could be blocked by excitation of the upper hypogastric nerves. Venous outflow studies demonstrated that the inhibitory effect of the sympathetic nervous system was due to active vaso- and corporeal smooth muscle constriction. It was concluded that subsidence and suppression of erection is a sympathetic function. Previous studies have shown that the neurophysiology of erection can be explained by 3 major inhibitory (sympathetic). Our findings are of clinical importance, since a better appreciation of the basic erectile mechanism is essential for successful management of erectile dysfunction.

Autonomic nervous control of cervical secretion in the guinea-pig.

Neurogenic influence on cervical secretion was studied in experiments performed on isolated guinea-pig cervix with intact adjacent nerves. The secretion was estimated as carbohydrate efflux. Experiments were undertaken at ovulation time when secretion is most prominent. Hypogastric nerve stimulation significantly increased carbohydrate release. This response was unaffected by phentolamine but inhibited by TTX, scopolamine and hexamethonium, as well as previous destruction of paracervical ganglia. Pelvic nerve stimulation did not affect cervical secretion. Carbachol as well as VIP induced a secretory response of the same extent as did hypogastric nerve stimulation. Scopolamine abolished the VIP-induced secretion. VIP and carbachol in combination had no additive effect. It is concluded that cervical glands of the guinea-pig uterus possess a cholinergic secretomotor innervation. The main pathway is the hypogastric nerve and neurons have a peripheral relay at paracervical ganglia. A more complex peripheral organization cannot be excluded.

TRH pharmacokinetics and nerve stimulation evoked prostatic fluid secretion during TRH infusion in the dog

The pharmacokinetics of TRH have been determined in man and the rat as well as other species whose serum contains TRH degrading enzymes, TRH pharmacokinetics have not been determined in the dog. This species is unusual in that its serum contains little or no TRH degrading activity. TRH pharmacokinetics were determined from measurements of plasma TRH concentrations during and following a 1-h infusion of TRH, 20 micrograms.kg-1.min-1, into dogs bearing prostatic urethral cannula. During TRH administration prostatic fluid secretion was evoked by hypogastric nerve stimulation and the content of TRH immunoreactive material in prostatic fluid was determined. Prostatic fluid was also collected after hypogastric nerve stimulation in dogs that did not receive TRH infusion. The TRH plasma profile in TRH-infused dogs exhibited two-compartment characteristics with an initial half-time of 10.4 +/- 5.4 (mean +/- SD) min, a terminal half-time of 69.4 +/- 24 min, and a metabolic clearance rate of 7.64 +/- 4.48 ml.min-1.kg-1. These findings suggest that the half-time of TRH is longer, and its metabolic clearance rate is less, in the dog than in humans or rats. TRH administration was not associated with altered nerve induced prostatic fluid secretion. Prostatic fluid samples contained TRH immunoreactive material regardless of whether they were collected after epithelial cell stimulation with pilocarpine, or after hypogastric nerve stimulation. In contrast to previous results with vasoactive intestinal peptide, TRH does not acutely alter prostatic fluid secretion. As has been reported for prostatic tissue extracts, immunoreactive material is present in prostatic fluid and appears to arise from epithelial cells.

Reorganization of sympathetic preganglionic connections in cat bladder ganglia following parasympathetic denervation.

1. Experiments were undertaken to examine the mechanisms involved in the reorganization of sympathetic efferent pathways to the urinary bladder of the cat following chronic unilateral, parasympathetic preganglionic denervation of the bladder. 2. Electrical stimulation (10-30 Hz) of the hypogastric nerve in cats with an intact bladder innervation or on the normally innervated side of the bladder in unilaterally denervated preparations elicited low-amplitude (10-25 cmH2O) transient (10-30 s) bladder contractions and non-synaptic axonal volleys on bladder postganglionic nerves. However, after chronic (3-22 months) sacral preganglionic denervation, hypogastric nerve stimulation on the side of the denervation elicited large (60-80 cmH2O) and more sustained (4-5 min) bladder contractions as well as synaptically mediated firing on bladder postganglionic nerves. 3. The vesicoexcitatory effects of hypogastric nerve stimulation on the chronically denervated side were not altered selectively by the adrenergic blocking agent, phenoxybenzamine, but were blocked by atropine and hexamethonium suggesting that the responses were mediated by muscarinic and nicotinic cholinergic synapses. These drugs did not influence the responses elicited by hypogastric nerve stimulation on the normally innervated side of the bladder. 4. Following more extensive chronic unilateral denervation (transection of the pelvic and hypogastric nerves on one side of the bladder) stimulation of the contralateral intact pelvic nerve elicited postganglionic firing in vesical postganglionic nerves on the denervated side. This crossed excitatory pathway was not observed in normal animals or following sacral preganglionic denervation. 5. It is concluded that parasympathetic preganglionic denervation of the bladder ganglia leads to a reinnervation of the denervated cholinergic ganglion cells by sympathetic preganglionic pathways in the ipsilateral hypogastric nerve. This reinnervation results in the conversion of sympathetic inhibitory pathways to excitatory pathways in the denervated bladder. This change may contribute to the development of the autonomous hyperactive bladder seen under conditions of peripheral nerve or conus medullaris lesions of the spinal cord.

Mechanical Responses of the Rat Uterus, Cervix, and Bladder to Stimulation of Hypogastric and Pelvic Nerves in Vivo1

Mechanical activities of the uterus, cervix, and bladder were recorded in vivo in anesthetized rats during electrical stimulation of either the hypogastric or pelvic nerve. Ovariectomized controls and hormone-treated groups were used as well as pregnant and postpartum rats. Stimulation of either hypogastric or pelvic nerve produced voltage- and frequency-dependent contractions of the three organs with no evidence of apparent inhibition. All evoked responses were completely abolished by tetrodotoxin, suggesting that these nerves are common pathways of innervation to the three organs. Atropine abolished uterine and cervical responses to both hypogastric and pelvic nerve stimulation, whereas bladder responses were only partly reduced. Hexamethonium almost totally blocked the evoked responses of the uterus and cervix. Phentolamine partly blocked uterine and cervical responses, and propranolol or physostigmine enhanced uterine and cervical responses to both hypogastric and pelvic nerve stimulation. These results suggest that motor innervation to the rat uterus and cervix is predominantly postganglionic cholinergic, with some alpha- and beta-adrenergic components, and that the bladder is innervated by mainly cholinergic and also noncholinergic nerves. Estrogen and estrogen-plus-progesterone pretreatment significantly increased the responses of uterus and cervix but not bladder. Uterine and cervical responses to either hypogastric or pelvic nerve stimulation were markedly reduced late in pregnancy and reappeared within 7 days after delivery.

Amphetamine antagonizes the presynaptic inhibitory effect of clonidine through an interaction at the level of the α2-adrenoceptors

1. 1. In the whole rat vas deferens 20 μM noradrenaline (NA) and 0.011 μM clonidine decreased (36 ± 7.4% and 80 ± 6.0% respectively) the motor response induced by hypogastric nerve stimulation. These effects were reverted by 1 μM yohimbine. Amphetamine 5.4 μM failed to antagonize the inhibitory effect of NA and attenuated clonidine effect. 2. 2. The effect of amphetamine was not altered by preincubation with either cocaine 1 μM, (−)-propranolol 0.3 μM or cocaine plus prazosin 0.028 μM. 3. 3. In reserpine pretreated animals amphetamine 5.4 μM shifted to the right the concentration-response curve (CRC) to clonidine 0.62 ± 0.05 log units with a KB value of 1.83 ± 0.30 μM. 4. 4. Binding of [ 3H]clonidine and [ 3H]prazosin were inhibited by amphetamine. Amphetamine was 90 times more potent to inhibit [ 3H]clonidine binding. 5. 5. The results obtained suggest a possible direct interaction between clonidine and amphetamine on α-adrenoceptor.

Parasympathetic depression of vas deferens contraction in the guinea‐pig involves adenosine receptors.

1. In the guinea-pig pelvic plexus-vas deferens preparation, stimulation of the parasympathetic pelvic nerves contracted the vas deferens then depressed the contractile responses to stimulation of the sympathetic hypogastric nerves. 2. The contraction caused by stimulation of the pelvic nerves was initially phasic then tonic. The contractions were almost abolished by application of hexamethonium to the plexus. The phasic contraction was abolished by alpha,beta-methylene adenosine triphosphate applied to the vas deferens. 3. Conditioning stimulation of the pelvic nerves preferentially depressed the phasic component of test contractions evoked by hypogastric nerve stimulation but did not affect the compound action potentials in postganglionic nerves evoked by test stimulation. 4. When the pelvic plexus was divided into two parts, one with the pelvic nerves and the other with the hypogastric nerves, conditioning stimulation of the pelvic nerves still depressed test contractions evoked by hypogastric nerve stimulation. 5. In the de-ganglionated vas deferens preparation, conditioning stimulation of some postganglionic nerves also depressed contractions evoked by test stimulation of the other postganglionic nerves. 6. 8-Phenyltheophylline (5-20 microM) applied to the vas deferens antagonized the conditioning stimulation-induced depression in both the pelvic plexus-vas deferens and the de-ganglionated preparations. 7. N6-Cyclohexyladenosine (CHA) and N6-(L-2-phenylisopropyl)-adenosine at 0.5 microM preferentially inhibited phasic contractions evoked by the postganglionic nerve stimulation. The effect of CHA was antagonized by 8-phenyltheophylline (10 microM). 8. The results indicate that the mechanism underlying the conditioning stimulation-induced depression of phasic contractions operates not in the ganglia, but through activation of adenosine receptors in the vas deferens.

Dynamic Study of Nervous Control on Prostatic Contraction and Fluid Excretion in the Dog

The effect of the section or stimulation of various nerves on prostatic contraction and fluid excretion was investigated dynamically in the dog using an apparatus devised in our laboratory.Prostatic contraction could be classified into two types from the pattern of the contracting wave. One was a prominent tonic contraction, designated as H-type contraction, observed typically after hypogastric nerve stimulation and followed always by prostatic fluid excretion. The other was a weak clonic contraction, designated as P-type contraction, occurring typically after pelvic nerve stimulation and accompanied by no fluid excretion.The periodical contraction of these two types was noticed even at rest. The H-type contraction was associated with fluid excretion with a mean rate of 0.3ml./hr. The denervation both of the hypogastric and pelvic nerves showed no distinct influence on contraction and excretion in the resting condition. The pudendal nerve was demonstrated to have no significant effect on prostatic contraction and fluid excretion.From these results, it was considered that dynamic fluid excretion followed by prostatic contraction was regulated chiefly by sympathetic fibers from the hypogastric nerve and the physiological role of parasympathetic fibers from the pelvic nerve was something other than fluid excretion.