Presence of serotonin in the rat vas deferens: its influence on contractile responses

Serotonin has been detected in the rat vas deferens. Increase in the serotonin concentration by exposure of the rat vas deferens to L-tryptophan occurs in vitro. p-chlorophenylalanine partly blocks the increase in serotonin concentration induced by tryptophan in vitro but not in vivo. Chronic sympathetic denervation induces an increase in 5-HT concentration. Responses of the vas deferens to transmural stimulation are depressed by pretreatment of rats with p-chlorophenylalanine, and the depression is reversed by incubation in vitro with 5-hydroxytryptophan or serotonin. Serotonin can enhance the response to transmural stimulation at low concentrations but has no effect at higher concentrations. Physostigmine-induced enhancement of the response to stimulation is depressed only by higher concentrations of serotonin. The results raise the question whether endogenous serotonin can act as a modulator of neurotransmission in the rat vas deferens.     

Role of calcium in the release of noradrenaline induced by sodium deprivation from the guinea-pig vas deferens

Summary The ability of Na-free media containing isotonic sucrose or equimolar choline chloride to increase the spontaneous release of noradrenaline from adrenergic nerve terminals and the dependence of the increase on extracellular calcium have been examined in the isolated guinea-pig vas deferens.The increase in noradrenaline output induced by the Na deprivation was gradual in contrast to the rapid response produced by excess potassium.The release of noradrenaline induced by the Na-free solution containing sucrose was not significantly reduced by the removal of calcium with or without EGTA in the first 1 h period, but was reversibly inhibited in the second 1 h period. On the other hand, the effect of the Na-free solution containing choline was significantly but reversibly decreased by exposure to the Ca-free media without any chelating agent in both periods of incubation.Lanthanum (0.25 mM) moderately inhibited the response induced by calcium reintroduction following exposure to the Ca-free, Na-free choline medium, but magnesium (10 or 20 mM) did not.It is suggested that Na deprivation may cause an increase in Ca influx, a decrease in Ca efflux or a release of intracellulary stored calcium resulting in an increase in the level of intracellular free calcium which then stimulates the output of noradrenaline.     

睾丸体积与输精管大小的活体测量

用木制的睾丸模型测量子,测定了要求作输精管结扎术的305例广东地区生育力正常男子609个睾丸的体积,结果是14.4±3.1ml,左右睾丸无显著差异.在305例中切出了170条输精管,在显微镜下进行了测量,外径为2.3±0.3mm,内径为0.5±0.1mm,相应的睾丸体积与输精管内、外径无显著相关.     

Dependence of contractile responses by some calcium antagonists on external calcium in the skeletal muscle

Dependence of contractile potentiation by calcium antagonists on external calcium was investigated on the frog's twitch muscle. Low concentrations (10(-6) to 10(-5) M) of nicardipine and verapamil enhanced the peak tension of both twitch and electrically induced contracture in the presence of calcium. In the calcium-free media the drugs suppressed the contractile tension. Caffeine contracture was inhibited by the calcium antagonists at 20 degrees C. This inhibition was caused by an early onset of relaxation, which was not observed at 7 degrees C. The results suggest that some interaction between calcium ions and drug molecules at the voltage sensor on the transverse tubular membrane, which regulates E-C coupling but is not directly related to the functional calcium channel, may play an important role for the phenomena. The inhibitory action of calcium antagonists on the caffeine contracture in the presence of calcium is probably independent of the potentiating effect seen in the depolarization-induced contractions.     

Intranuclear inclusions of the human vas deferens.

Intranuclear inclusions in epithelial cells of the human vas deferens have not been well characterized or widely recognized. We studied their prevalence in an adult male population by light microscopy and characterized them using the techniques of histochemistry, electron microscopy, and electron microprobe analysis. They occurred in all cases studied, consisted of electron dense globules, contained neutral mucosubstances, and occasionally were single membrane bound. Epithelial intranuclear inclusions routinely occur in the vas deferens of sexually mature males, do not disappear with advancing age, and should not be interpreted as a pathologic finding.     

Co-transmission in the rat vas deferens: postjunctional synergism of noradrenaline and adenosine 5'-triphosphate

In the isolated prostatic half of the rat vas deferens, joint application of noradrenaline (NA) and adenosine 5'-triphosphate (ATP) produced a contractile response whose magnitude was greatly larger than the addition of the tension generated by the application of each agent alone. The effect of ATP was mimicked by two non-hydrolyzable ATP analogs, but not by GTP, AMP or adenosine. In sympathectomized rats, ATP potentiated NA effects, increasing both the peak tension and the duration of the vas deferens contractile response. The synergism was concentration related. Prazosin antagonized the NA synergism but not the ATP response. Likewise, desensitization of the P2-purinoceptor blocked the ATP synergism without modifying the NA-induced contraction.     

Dual excitatory actions of acetylcholine at the neuromuscular junction in the guinea-pig vas deferens

The action of acetylcholine (ACh) on the smooth muscle of guinea-pig vas deferens was studied using the sucrose-gap method. ACh, when applied at a concentration of 10^–6 M, evoked a depolarization of the smooth muscle membrane which was slow in time course (slow depolarization). When ACh was applied at higher concentrations, another depolarization which was fast in time course (fast depolarization) occurred, overlapping the early part of the slow depolarization. The magnitudes of both depolarizations were concentration-dependent on ACh. TTX and adrenergic receptor antagonists had little effect on either depolarizations, while guanethidine and nicotinic receptor antagonists mainly suppressed the fast depolarization. In contrast, atropine suppressed the slow depolarization. The membrane conductance observed by current application, was reduced during the slow depolarization, and the reversal potential of the depolarization was 18.3 mV negative to the resting membrane potential. Whereas, the reversal potential of the fast depolarization was 27.6 mV positive to the resting membrane potential. This reversal potential was quite similar to that of the adenosine triphosphate (ATP)-induced depolarization, previously observed in the same tissue. From these observations, it is suggested that in the guinea-pig vas deferens, ACh acts on nicotinic receptors at the sympathetic postganglionic nerve terminal, causing the release mostly of a non-adrenergic transmitter, probably ATP. In addition, ACh also acts on muscarinic receptors on the smooth muscle membrane, inducing membrane depolarization resulting from a reduction of the membrane conductance to potassium ions.     

Decrease in membrane conductance induced by noradrenaline in the smooth muscle of guinea-pig vas deferens

The electrical response of the smooth muscle of guinea-pig vas deferens to exogenously applied noradrenaline (NA) was examined using the double sucrose-gap method. NA evoked a depolarization of the smooth muscle membrane which was associated with an increase in the size of electrotonic potentials. A conditioning depolarization of the membrane induced by current application enhanced the size of NA-induced depolarization, whereas a conditioning hyperpolarization reduced it. When a conditioning hyperpolarization of 25 mV in magnitude was applied, the direction of potential change induced by NA was reversed. These results are discussed with respect to the ionic mechanism of the electrical event in response to NA in this tissue.     

The relation between in vitro efflux of noradrenaline from platelets and vas deferens in man

The efflux of isotope-labelled noradrenaline from platelets and vas deferens was compared in 29 healthy males. Platelets and a preparation of tissue from vas deferens were incubated with isotope-labelled noradrenaline until equilibrium in the uptake was obtained. The spontaneous efflux of noradrenaline in buffer was measured for 20 min. There was a significant positive correlation between the efflux of noradrenaline from platelets and vas deferens (r = 0.56, P less than 0.001).     

Presynaptic inhibitory actions of adenine nucleotides and adenosine on neurotransmission in the rat vas deferens.

Adenine nucleotides and adenosine inhibited the isometric contractions of the rat vas deferens in vitro in response to field stimulation but had no effect on the responses to exogenous noradrenaline. The inhibitions were potentiated by dipyridamole and compound 555, antagonized by theophylline and unchanged by indomethacin, 2-2′-pyridylistogen, phenoxybenzamine and atropine. Adenosine and adenosine 5′-triphosphate inhibited the release of [³H]noradrenaline produced by field stimulation.These results indicate that adenine nucleotides, probably acting via the common metabolite adenosine, inhibit adrenergic neurotransmission at a presynaptic site. Their antagonism by theophylline suggests that a presynaptic ‘purinergic’ receptor system could be involved.     

Post- and prejunctional consequences of ecto-ATPase inhibition: electrical and contractile studies in guinea-pig vas deferens

At sites of purinergic neurotransmission, synaptic ecto-ATPase is believed to limit the actions of ATP following its neural release. However, details of the modulation by this enzyme of the ATP-mediated conductance change and the possible mechanisms mediating this modulation remain unelucidated. We have addressed these issues by studying the effect of ARL 67156, a selective ecto-ATPase inhibitor, on ATP-mediated electrical and contractile activity in the sympathetically innervated guinea-pig vas deferens. ARL 67156 at 100 μ m significantly potentiated the amplitude of spontaneous excitatory junction potentials (SEJPs) by 81.1% ( P < 0.01) and prolonged their time courses (rise time by 49.7%, decay time constant by 38.2%; P < 0.01). Moreover, the frequency of occurrence of SEJPs was strikingly increased (from 0.28 ± 0.13 to 0.90 ± 0.26 Hz; P < 0.01), indicating an additional, primarily presynaptic, effect of ecto-ATPase inhibition. The frequency of occurrence of discrete events (DEs), which represent nerve stimulation-evoked quantal release of neurotransmitter, was also increased (∼6-fold; P < 0.01), along with the appearance of DEs at previously 'silent' latencies. Purinergic contractions of the vas deferens were potentiated significantly ( P < 0.01) by ARL 67156; these potentiated contractions were suppressed by the A1 agonist adenosine ( P < 0.01) but left unaffected by the A1 antagonist 8-phenyltheophylline (8-PT). Our results indicate (i) that ecto-ATPase activity, in addition to modulating the ATP-mediated postjunctional conductance change, may regulate transmitter release prejunctionally under physiological conditions, and (ii) that the prejunctional regulation may be mediated primarily via presynaptic P2X, rather than A1, receptors.