Electrical activity from smooth muscle of the anal sphincteric area of

J. Physiol. (1981), 310, pp. 445-456 445With 9 text-ftgure8Printed in Great Britain

ELECTRICAL ACTIVITY FROM SMOOTH MUSCLE OF THE ANALSPHINCTERIC AREA OF THE CAT

BY M. BOUVIER AND J. GONELLAFrom the Department de Neurophysiologie Vegetative, Institut de

Neurophysiologie et Psychophysiologie, C.N.R.S., 31 chemin Joseph Aiguier,13274 Marseille, Cedex 2, France

(Received 17 December 1979)

SUMMARY

1. The electrical activities of longitudinal and circular smooth muscle of the analsphinteric area have been studied in the cat.

2. Electromyographic recordings were achieved with extracellular electrodes,in vivo on acute and chronic animals, and in vitro on the isolated organ. In addition,electrical and mechanical activities were recorded from muscle strips with thesucrose gap technique.

3. Circular muscle coat electrical activity consisted exclusively of slow variationsof the membrane potential of the smooth muscle cells. Each slow potential variationwas followed by a contraction.

4. The electrical activity and the concomitant contractions were tetrodotoxinresistant (10-6 g/ml.). Both disappeared in Ca-free solution or in the presence of Mnions (10-3 M).

5. On circular muscle, noradrenaline (10-8-10-7 g/ml. in vitro, or 0 1-0'15 mg/kgin vivo) had an excitatory effect consisting in an increase of slow potential frequency.The action of noradrenaline was antagonized by phentolamine (10-6f-10- g/ml. invitro, or 0-2 mg/kg in vivo).

6. On circular muscle, acetylcholine (10-8-10-6 g/ml.), used exclusively on musclestrips, did never produce any clear cut effect.

7. Longitudinal muscle coat electrical activity consisted of spike potentials super-imposed on slow time course depolarizations which were never observed alone. Eachspike was followed by a contraction. This electrical activity was tetrodotoxinresistant (10-6 g/ml.).

8. Longitudinal muscle activity was abolished by noradrenaline (10-6 g/ml.) andenhanced by acetylcholine (10-8-10-6 g/ml.). The action of noradrenaline wasantagonized by propranolol (0-2 mg/kg i.v.; 10-6 g/ml.) and that of acetylcholine byatropine (10-7 g/ml.).

9. Electrophysiological and pharmacological data indicate that electromechanicalcoupling is achieved (1) in circular muscle, through Ca dependent slow variations inmembrane potential of the muscle cells and (2) in longitudinal muscle, through spikepotentials. Noradrenaline has opposite effects on the two muscle coats: circularmuscle is excited through a-receptors located on muscle cells membrane: longi-tudinal muscle is inhibited through f-receptors. Acetylcholine excites longitudinalmuscle through muscarinic receptors, but it has no effect on circular muscle.

0022-3751/81/2890-0670 $07.50 © 1981 The Physiological Society

M. BOUVIER AND J. GONELLA

INTRODUCTION

It is assumed (see Schuster, 1968) that the internal anal sphincter contributesmostly to the pressure recorded inside the anal canal. Anatomically, in the cat, thesmooth muscle sphincteric area does not differ from the adjacent part of the gut.However it has been shown (Langley & Anderson, 1895) that sympathetic nervestimulation produces a contraction of the internal anal sphincter, and in contrast, arelaxation of the rectum. Most of the investigations have been performed using mano-metric techniques (see Schuster, 1968; Garrett, Howard & Jones, 1974). Morerecently the internal anal sphincter has been studied using the electromyographictechnique, in guinea-pig (Costa & Furness, 1973), cat (Kerremans & Penninckx, 1970)and man (Kerremans, 1968; Ustach, Tobon, Hambrecht, Bass & Schuster, 1970;Taylor, Smallwood & Duthie, 1973; Naudy, Ranieri, Salducci & Monges, 1976).From those last studies, it appears that the nature of the electrical activity of theanal sphincter as well as the relationship between the electrical and mechanicalactivities remain unclear and controversial.The present work was performed in order to determine (1) the characteristics of

the electrical activity of the sphincteric smooth muscle fibres (external longitudinaland internal circular layers) and (2) the relationship between the electrical andmechanical activities of those muscle fibres. These points being clarified, the sphinc-teric motility has been studied using the electromyographic activity alone, in orderto avoid any disturbance due to the presence of a catheter or a balloon in the analcanal.

METHODS1. AnatomyIn the cat, the internal anal sphincter, about 10 mm long, is the most distal part of the

circular layer of the gut. Its proximal side is in continuity with the circular layer of the rectum,and its distal side attached to the skin. On visual examination the spinster exhibits a greaterpermanent tonic contraction than the rectum. The same continuity between the rectum and thespincteric area exists for the longitudinal smooth muscle, the distal part of which is also attachedto the skin. However when the longitudinal muscle reaches the beginning of the sphincteric area(i.e. the limit between the circular muscle of the rectum and the sphincter itself), it divides intowell individualized bundles 0-5-0-8 mm wide (Fig. 1). These bundles are attached one to anotherand also to the subjacent circular layer, by a very loose connective tissue. On the lateral partsofthe sphincter, the longitudinal muscle is more or less intermingled with bundles of an accessorymuscle of defaecation, the ano-coccygeus muscle.

Before dissection of longitudinal muscle strips, the ano-coccygeus muscle was removed. Thusthe part of the bundle from which electrical activity was recorded was actually part of thelongitudinal muscle of the sphincteric area, in continuity with the longitudinal muscle of therectum.

2. In vivo experimentsFifty-two cats of either sex (2-4 kg) were used in acute experiments. The trachea was cannu-

lated and a polyethylene catheter was inserted into the radial vein under halothane (2%)anaesthesia. Then the concentration of halothane was decreased and the animal was perfusedI.v. with a Na thiopentone (Nesdonal, SPECIA, Paris) solution using a peristaltic pump. The rateof the pump was adjusted to 6 ml./hr, the concentration of the anaesthetic given to the animalbeing 20 mg/kg.hr. The depth of anaesthesia was verified by the absence of palpebral reflex.The level of anaesthesia was stable throughout the experiment. The body temperature wasmaintained at 37 0C.

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SMOOTH MUSCLE ANAL SPHINCTERThe sphincteric zone was exposed after a vertical incision (2-3 cm long) between the anal

margin and the base of the tail. The striated external anal sphincter was then divided by a dorsalincision and reclined on both sides of the anal canal. Electrical activity was recorded usingexternal pressure electrodes as previously described (Gonella, 1972). e.m.g. was recorded on achart-strip recorder with AC amplifier (band pass 0-120 Hz; time constant 2-5 sec). It had beenpreviously verified by using selective filters that the recording apparatus was suitable for smoothmuscle spikes recording. In chronic experiments (n = 3), 041 mm insulated wires of a Ni-Cralloy (21 % Cr) were implanted in the circular muscle following the method of Basmadjian &Stecko (1962). The wires were tunelled under the skin and soldered to a connector fixed on theskull with cement. All the surgical preparations were performed under Nembutal anaesthesia(30 mg/kg i.P.) and under aseptic conditions. Electrical activity was recorded under bipolarconditions (distance between the electrodes 2-3 mm).

RFig. 1. Schematic representation of the smooth muscle layers in the anal sphinctericregion. S sphincteric area R rectum LM longitudinal muscle CM circularmuscle: mu = mucosa.

3. In vitro experiments

Following a brief induction with halothane (2%), cats (n = 7) were anaesthetized with Nathiopentone (Nesdonal, 10% i.v.). The sphincteric region was excised with a part of rectum(1-2 cm long) and placed horizontally in an organ bath perfused with saline solution of thefollowing composition (mM): NaCi = 133; KCl = 4-7; CaCl2 = 1-9; MgCl2 = 0-49; NaH2PO4 =1-0; glucose = 7-8. The solution was bubbled with a 95% 02 and 5% CO2 gas mixture andmaintained at 36 0C. When the ionic composition was modified, the osmolarity was kept constantby adding or removing an equivalent quantity of NaCl. The recording technique was the same asthat previously described for in vivo experiments.

4. Sucrosee gap experimentsAfter the surgical phase previously described in the preceding chapter, the muscle (forty-two

circular and thirteen longitudinal) strips were mounted in a double sucrose gap apparatus similarto that used by Biilbring &s Tomita (1969) and detailed by Szurszewski (1973). The musclestrips were 30-35 mm long with a diameter of 0-6-0-9 mm. In the isotonic K2504 solution themuscle strips was 3-4 mm long and (15mm in the gap containing isotonic sucrose). The salinegap width was 0-6-0-9 mm. The remaining part of the muscle strip was placed in a second gap ofsucrose to avoid its activity. The sucrose solution was deionized by its passage on a column ofresin (Amberlite MB3); Ca ions were not added. The recordings were obtained after 20-30 mmn ofequilibration. The muscle strip was kept inside the sucrose gap up to 2 hr, even though weensured that the reactivity of the muscle strips to various drugs lasted for longer periods of time.The longitudinal muscle of the sphincteric area (10 mm) is too short compared to the length

of muscle strips necessary (30 mm) for the double sucrose gap. For this reason a part of rectallongitudinal muscle (20-10 mm long) was also cut off. However the muscle strip was placed insidethe sucrose gap apparatus in such a way that the muscle located in the gap saline solution was

447


that of the sphincteric area. The most proximal part (attached to longitudinal muscle of therectum) being partly in sucrose and partly in K2S04 solutions. The electrical activity wasrecorded by Ag-AgCl electrodes (between the saline and the K2SO solution, ground electrodebeing in contact with saline liquid vein) and displayed on one beam of a cathode ray oscilloscopeby means of a cathode follower (Clottes, 1969). Variations of tension were recorded using amechanical transducer (Talbot, Lilienthal, Beser & Reynolds, 1951) connected to the secondbeam of the oscilloscope. Electrical and mechanical activities were amplified with DC amplifiers(band 0-200 kHz). Oscilloscope tracings were photographed by a camera attached to theoscilloscope.Atropine and eserine were obtained from Boyer & Co. (Paris), propranolol, acetylcholine, nor -

adrenaline (L-Arterenol HCl) from Sigma Chemical (Saint Louis, Mo.), tetrodotoxin from Sankyo(Tokyo), and phentolamine (Regitine) was kindly supplied by CIBA (Paris).

A

1 mV20 sec

B

C 20Isec 1mV

Fig. 2. Circular muscle e.m.g. recorded from acute (A and B) and chronic (C) prepara-tions. Each pair of tracings represents a continuous record. A and B were obtainedfrom two different animals using monopolar pressure electrodes. C is a bipolar recording.Time constant of the amplifier: 2-5 sec. Note the variations of amplitude oscillations:large in A, small in C and almost non existent in B.

RESULTS

1. Electrical activityfrom the circular layer: recordings on acute and chronicpreparationsA. Acute preparations. Recording electrodes were placed directly on the circular

layer after spreading out two bundles of longitudinal muscle. In most experiments(90 %; n = 52) a spontaneous oscillatory activity was recorded. It consisted of asuccession of slow potentials variable in frequency and amplitude (Fig. 2 and Table 1)and presented sometimes a waxing and waning pattern. This frequency varied alongthe recording period and ranged from 9 to 30 cycles per minute. Table 1 indicates thefrequency ranges recorded from ten animals for up to 100 min before injection of anydrug. Simultaneous recordings, with several electrodes distant from 2 to 3 mm andparallel to the sphincteric axis, indicated that the electrical activity propagated in an

448

SMOOTH MUSCLE ANAL SPHINCTER 449

aboral-oral direction (Fig. 3); a propagation in the opposite direction has never beennoticed. When such a propagated activity was present, visual observation indicatedthe occurrence of antiperistaltic contractions.

B. Chronic preparations. All the animals (n = 3) exhibited a spontaneous activity.Table 2 indicates that the slow potential frequency (26-34 c/min) was more stablethan in acute preparations. This difference between acute and chronic preparationsmight be attributed to eventual nervous influences which are difficult to control inanaesthetized preparations.

TABrE 1. Frequency of the spontaneous electrical activity within the circular muscle layer ofthe internal anal sphincter in vivo on acute animals (n = 100)

Cat C/min Range ofno. (mean + s.E.) values1 24-53±0.30 18to302 23-29 0-29 18 to 303 22.7 +0.28 18 to 294 22-51+ 0.32 18 to 305 22*34+0-16 19 to 296 17*07 + 0*22 12 to 217 14.2 + 0-25 9 to 218 14-13±0-17 9to 179 13-21+0.3 9to 17

10 13 ±0-16 9 to 16

| | ~~~~~~~~~05 mV

2\

3

5 secFig. 3. Simultaneous circular muscle e.m.g., recorded from acute preparations withthree pressure electrodes. 1: distal electrode (near the skin attachment); 3: proximalelectrode (near to rectum); 2: intermediate electrode. Notice the retrograde propagationof electrical activity. The incidental modifications of the frequency occurring on trace 1(between 4th and 5th, 6th and 7th potentials) appear on traces 2 and 3, with increasingdelay, this indicates that the electrical activity was generated by a pacemaker locatednear the 1st electrode and that it propagates toward the proximal part of the sphincter.Time constant of amplifiers: 2-5 sec.

2. Recording from circular muscle using sucrose gap methodSpontaneous slow potentials, similar to those obtained in vivo by extracellular

electrodes, were recorded with the sucrose gap technique in 74% of the strips(n = 42). The other strips (26 %) had no spontaneous activity. Each slow potentialwas followed by a contraction (Fig. 4). Slow potentials were not abolished by tetrodo-toxin (10-6 g/ml.) indicating that this spontaneous activity was myogenic.

I5 PHY 310


In Ca-free solution (Fig. 5) or when manganese ions (1 x 10-3 M) were added to thesaline solution (Fig. 6), the electrical and mechanical activities disappeared within20-30 sec. Recovery occurred 30 see -1 min after washing out with normal salinesolution. After suppression of manganese ions, both electrical and mechanicalactivities reappeared within 15-30 see with generally an irregular pattern.

TABLE 2. Frequency of the spontaneous electrical activity within the circular muscle layer ofthe internal anal sphincter on chronically implanted animals (n = 10)

Cat C/min Range ofno. (mean ± s.E.) values

1 28 3±037 26 to 302 30.2 + 0-71 27 to 343 30 3 ± 0-96 26 to 34

55 mg

1 0 sec 5 mV

Fig. 4. Spontaneous electrical and mechanical activities of a circular smooth musclestrip (sucrose gap technique). The bottom pair of traces follows the top traces withoutany interruption. In each pair of traces: upper trace: mechanical activity; lower trace:electrical activity. Note the relationship between slow membrane depolarizations andmuscular contractions.

3. Effects of acetylcholine, eserine and noradrenaline on the activity of the circular muscleAcetylcholine (10-8-10-6 g/ml.), exclusively used on muscle strips, (eighteen strips

from fifteen animals) produced slight increases or decreases in the frequencymembrane potential oscillations. No effect was observed on non-spontaneously activepreparations. Eserine (10-7 g/ml.) on isolated organs caused a decrease (about 25%)in frequency membrane potential oscillations; no detectable effect was observed aftereserine (0.1 mg/kg) on in vivo preparations.On spontaneously active preparations, noradrenaline produced, at threshold

concentrations (10-8- 1 0-7 g/ml.), an increase in frequency and amplitude of themembrane potential oscillations (Fig. 7, upper record and Table 3). With higher doses(above 10-7g/ml.) a sustained depolarization with superimposed oscillations wasobserved (Fig. 7, lower record). On non-spontaneously active preparations, nor-adrenaline gave rise to oscillations or to gradual long-lasting depolarization withoutany superimposed oscillation. On in vivo preparations, noradrenaline (0 1-0.15 mg/kg)caused an increase in frequency membrane potential oscillations. In all the prepa-rations (in vivo and in vitro) the effects of noradrenaline were antagonized by phentol-

450

SMOOTH MUSCLE ANAL SPHINCTER

amine (in vitro: 10-5-10-6 g/ml.; in vivo: 0'2 mg/kg i.v.) indicating that the excita-tory effect of noradrenaline is mediated through a-receptors.

4. Electrical activity from the longitudinal layerOn in vivo preparations and isolated organ, the e.m.g. was characterized by phases

of spontaneous activity (i.e. which appears without any experimental intervention)interrupted by irregular periods of electrical silence lasting from 3 see to 7 min. Thespontaneous electrical activity consisted of a slow component with usually one, oroccasionally two, spikes superimposed. The slow component was never observed alone(Fig. 8). The amplitude of both components could vary at the same recording site(Fig. 8).

55 mg

A

B

10 sec

CA..

Fig. 5. Effect of Ca deprivation on spontaneous electrical and mechanical activitiesof a circular muscle strip. In A, B and C, upper trace: mechanical activity; lower trace:electrical activity. Ca-free solution has been applied in A between arrows. B and C:respectively 65 and 115 see after washing out with normal physiological solution. Notein B (for the three first contractions) the relationship between the two electrical andmechanical components. The limit between the mechanical components is indicatedby oblique arrows. This peculiar electrical activity might correspond to that of twomuscle bundles having the same frequency but being somewhat out of phase. When thephase lack decreases, its effect on mechanical activity is minimized.

With the sucrose gap technique (thirteen strips from eleven animals), a similarspontaneous electrical activity, previously described for in vivo preparations andisolated organs has been recorded (Fig. 9). In addition it was observed that eachspike was followed by a contraction (Fig. 9). When a spontaneous activity wasobserved (four strips), tetrodotoxin (10-6 g/ml.) failed to abolish it.In vivo, noradrenaline (0 15-0 10 mg/kg i.v.) abolished the spontaneous muscle

activity. On muscle strips, noradrenaline (up to 10-6 g/ml.) decreased the duration ofthe spontaneous discharge (Fig. 9C). At higher concentrations (above 10-6 g/ml.)the spontaneous activity was immediately abolished. This inhibitory effect, only seenin spontaneously active preparations, consisted of an early repolarization of the

15-2

451


smooth muscle fibres (Fig. 90). Noradrenaline did not hyperpolarize either spon-taneously active smooth muscle fibres or those which had a stable membranepotential (e.g. when the noradrenaline was applied during periods of electricalinactivity). The inhibitory effect of noradrenaline on spontaneously active prepa-rations was antagonized by propranolol (0-2 mg/kg i.v.; 10-6 g/ml., in vitro),indicating that this inhibitory effect was mediated through f-receptors.

A 55 mg

_~~~10 mV

110sec

Fig. 6. Effect of manganese ions on spontaneous electrical and mechanical activity ofa circular muscle strip. In A, upper trace: mechanical activity; lower trace: electricalactivity. In B, lower trace: mechanical activity; upper trace: electrical activity.Mg ions were added in A between arrows. Recordings were interrupted 15 see betweenA and B. Recovery after Mn is less complete than after Ca-free solution (see Fig. 5).

TABLE 3. Excitatory effect of noradrenaline on the spontaneous electrical activity within thecircular muscle layer of the internal anal sphincter in vitro*

During the action ofControl noradrenaline

14-75 + 2-59 24-75 + 2-59 (17-38)(8-27) P < 0.001 t test for

paired values (n = 8)* For threshold concentrations of noradrenaline varying from 1.10-8 to 1 10-7 g/ml. Numbers

are mean values of the frequency of electrical activity in c/min ± s.E. with the range of valuesprovided in parentheses.

Acetylcholine (10-8-10-6 g/ml.), on spontaneously active muscle strips (n = 14;eleven animals), prolonged the discharge of slow and spike potentials (Fig. 9B). Innon-spontaneously active muscle strips, acetylcholine (10-s-10-6 g/ml.) induced adischarge of slow potentials and superimposed spikes. The excitatory effect ofacetylcholine was mediated through muscarinic receptors since it was antagonized byatropine (10-7 g/ml.). The effect of acetylcholine was unaffected by tetrodotoxin(10-6 g/ml.) indicating that it was not neurally mediated.

452


Eserine (1 mg/kg, I.v. or 5 x 10-7 g/ml., in vitro) in vivo or on isolated preparations,in the absence of any nerve stimulation, produced a continuous and fairly regulardischarge of slow potentials and spikes. This excitatory effect was antagonized byatropine (0.1 mg/kg, i.v.; or 10-7 g/ml. in vitro) indicating that in these preparationsthe muscle activity may be modulated by nerves.

A1 0 sec

Fig. 7. Action of noradrenaline on the spontaneous electrical activity of a circularmuscle strip (sucrose gap technique). The muscle strip was treated by tetrodotoxin(10-6 g/ml.) 25 min before the recording. A and B were obtained from the same stripat different times. The application of noradrenaline (10-7 g/ml. in A and 10-6 g/ml.in B) is indicated by the black line under each tracing. Note on both records the increasein frequency leading to a synchronization of electrical activity, and on bottom tracethe sustained depolarization with superimposed oscillations.

A

1 mV

5 sec

B

5 secFig. 8. Electrical activity of longitudinal muscle. In vitro on the isolated organ (A)an4 in vivo on acute preparation (B); the three spike potentials were recorded at thesame site. Note that the spike potential component was always present but sometimesincompletely developed.

DISCUSSION

The correlations between mechanical and electrical activities indicate that in thecircular smooth muscle of the anal sphincter, the electromechanical coupling isachieved through slow time course variations in the membrane potential of thesmooth muscle cells. The suppression of cyclic activity in calcium free solution orwhen manganese ions, which block the Ca conductance of smooth muscle fibres(Hagiwara & Nakajima, 1966) are present in normal physiological solution, indicatesthat the slow depolarizations are Ca dependent.

It must be pointed out that the spontaneous depolarizations of sphincteric smooth

453


muscle are different from the slow waves of the small intestine (Gonella, 1970; ElSharkawy & Daniel, 1975) and the colon (Christensen, Caprilli & Lund, 1969;Gonella & Gardette, 1974) which never give rise to contractions. The slow depolariza-tion of the circular sphincteric muscle presents some analogy with the slow componentof the canine gastric action potential (Papasova, Nagai & Prosser, 1968; Szur-szewski, 1975) and that of the guinea-pig ureter (Shuba, 1975) the amplitude of whichdetermines the strength of the contraction.

Control

A

Acetylcholine 1 x 1 0-8 g/ml.

B

Noradrenaline 1 x 106g/ml. 20sec

C

Fig. 9. Effect of acetylcholine and noradrenaline on spontaneous electrical andmechanical activities of the longitudinal muscle (sucrose gap technique). For A, B andC, upper record: mechanical activity; lower record: electrical activity. B recording wasperformed in physiological solution containing acetylcholine 10-8 g/ml. Noradrenaline(10-6 g/ml.) was applied during the time indicated by the black line under C electricalrecord. Acetylcholine increases the duration and frequency of action potentials. Incontrast, noradrenaline shortens this discharge and causes an early muscle membranerepolarization. The action potential component was not regularly fully developed buthowever sufficient to reach the mechanical threshold and trigger a contraction.

Recordings obtained with the sucrose gap technique indicate that the tone insphincteric muscle is related to the frequency of the slow depolarizations. Theincrease of the slow depolarization frequency is associated with an increment oftension which produces an incomplete tetanus of sphincteric muscle (see Fig. 5).In addition the efficiency of the sphincter closure, and hence its holding capacity, ispresumably reinforced by the propagation of the electrical activity in the aboral-oraldirection. A similar propagation of the sphincteric electrical activity has been ob-served in man by Kerremans (1968). The data indicates that a pace-maker ofsphincteric electrical activity is probably located near the area of circular muscleattachment on the skin.

Noradrenaline has a direct excitatory effect, mediated through a-receptors locatedon the circular smooth muscle cells, this result confirming the data obtained by otherauthors (Garrett et al. 1974). Acetylcholine and cholinomimetic drugs have no direct

454


effect on circular muscle. The slight and inconstant action, observed only on spon-taneously active preparations, may be attributed to an effect mediated throughnervous structures; this result is in agreement with that of Garrett et al. (1974) onthe cat.As far as longitudinal muscle is concerned, electrical activity and reactivity

towards acetylcholine and noradrenaline are those usually described for longitudinalmuscle in most parts of the digestive tract. From a functional point of view it mustbe noted that (1) noradrenaline inhibits longitudinal muscle while it excites circularmuscle, (2) acetylcholine excites longitudinal muscle whereas it has no direct effect oncircular muscle. These two opposite effects are probably related to their differentfunctions during defaecation. During the expulsion phase, the sphincter (i.e. circularmuscle) relaxes while the contraction of the longitudinal muscle, which appears to bean extension of the longitudinal layer of the rectum, would contribute to an openingof the sphincter and to some extent to an eversion of the mucosa by a traction on theskin around the anal orifice. In digestive tract smooth muscles of most mammals,the response to stimulation of adrenergic receptors is generally inhibitory, except forsphincter smooth muscle. Thus early data of the literature (Langley & Anderson,1895; Carlson, 1922) indicate that in the internal anal sphincter and in the loweroesophageal sphincter the stimulation of adrenergic receptors has an excitatoryeffect. However the comparison of our own results with those presented recently byGonella, Niel & Roman (1979) indicates that the excitatory mechanism of nor-adrenaline is different in the two sphincters. In the anal sphincter, noradrenaline hasa direct effect on smooth muscle, whereas in the lower oesophageal sphincter, nor-adrenaline acts through a cholinergic nervous mechanism, since the motor action ofnoradrenaline is antagonized by atropine (Christensen & Daniel, 1968; Gonella et al.1979). Another difference lies in the action of acetylcholine which has a directexcitatory effect on lower oesophageal smooth muscle (Christensen & Daniel, 1968;Gonella et al. 1979) whereas it has no effect on anal sphincter smooth muscle.

We are grateful to Dr Y. Jule for his helpful discussion and criticism of draft of the manu-script. Thanks also to Mrs F. Farnarier for her help in the preparation of the manuscript and toMrs P. Rouviesre for her skilful technical assistance.

REFERENCES

BASMADJIAN, J. V. & STECKO, G. (1962). A new bipolar electrode for electromyography. J. appt.Physiol. 17, 849-852.

BULBRING, E. & TOMITA, T. (1969). Increase of membrane conductance by adrenaline in thesmooth muscle of guinea-pig taenia coli. Proc. R. Soc. B 172, 89-102.

CARLSON, A. J. (1922). The innervation of the cardia and the lower end of the esophagus inmammals. Am. J. Physiol. 61, 14-41.

CLOTTES, A. (1969). Abaisseur d'impedance pour enregistrement des potentials physiologiquespar micro6lectrodes neutres ou polarisees. Electronique medical 53, 93-95.

COSTA, M. & FuRNEss, J. B. (1973). The innervation of the internal anal sphincter of the guinea-pig. Proc. I Vth international Symposium on Gastrointesttnal Motility (Banff, Canada), pp. 681-690. Vancouver: Mitchell Press.

CERISTENSEN, J., CAPRILLI, R. & LUND, G. F. (1969). Electric slow waves in circular muscle ofcat colon. Am. J. Physiol. 217, 771-776.

CRISTENSEN, J. & DANIEL, E. E. (1968). Effects of some autonomic drugs on circular oeso-phageal smooth muscle. J. Pharmac. exp. Ther. 159, 243-249.

455


EL SHARKAwI, T. & DANIEL, E. E. (1975). Ionic mechanisms of intestinal electrical controlactivity. Am. J. Physiol. 229, 1287-1298.

GARRETT, J. R., HOWARD, E. R. & JONES, W. (1974). The internal anal sphincter in the cat:a study of nervous mechanisms affecting tone and reflex activity, J. Phy&iol. 243, 153-166.

GoNELLA, J. B. (1970). Etude de l'activit6 6lectrique de la couche longitudinale du duod6numde Lapin. J. Physiol., Paris 62, 447-476.

GoNELLA, J. B. (1972). Modifications of electrical activity of the rabbit duodenum longitudinalmuscle after contractions of the circular muscle. Am. J. dig. Dis. 17, 327-332.

GONELRA, J. B. & GARDETTE, B. (1974). Etude in vivo de la commande nerveuse extrins~queparasympathique du c6lon. J. Physiol., Paris 68, 393-415.

GoNEIA, J. B., NIEL, J. P. & ROMAN, C. (1979). Sympathetic control of lower oesophagealsphincter motility in the cat. J. Physiol. 287, 177-190.

HAGIWARA, S. & NAKAJIMA, S. (1966). Differences in Na and Ca spikes as examined by appli-cation of tetrodotoxine, procaine and manganese ions. J. gen. Physiol. 49, 793-806.

KERREMANs, R. (1968). Electrical activity and motility of the internal anal sphincter. Actagastroenterol. belg. 31, 466-482.

KERREMANS, R. & PENNINcKX, F. (1970). A study 'in vivo' of adrenergic receptors in therectum and in the internal anal sphincter of the cat. Gut 11, 709-714.

LANGLEY, J. N. & ANDERSON, H. (1895). On the innervation of the pelvic and adjoining viscera.Part I. The lower portion of the intestine. J. Physiol. 18, 67-105.

NAUDY, B., RANIERI, F., SALDUCCI, J. & MONGES, H. (1976). Etude electromyographique durectum et du sphincter anal interne chez l'Homme au cours du reflexe recto-sphincterieninhibiteur. J. Physiol., Paris 72, lllA.

PAPASOVA, M. P., NAGAI, T. & PROSSER, C. L. (1968). Two-component slow waves in smoothmuscle of cat stomach. Am. J. Physiol. 214, 695-702.

ScHiuSTER, M. M. (1968). Motor action of rectum and anal sphincters in continence and defe-cation. In Handboolk ofPhysiology, section 6: alimentary canal. vol. iv, Motility, ed. C. F. Code.Washington, D.C.: American Physiological Society.

SHUBA, M. (1975). Mechanism of action of catecholamines and histamine on smooth muscle cellsof guinea-pig ureter. J. Physiol. 245, 88P.

Szu szEwsK, J. H. (1973). Recording of electrical activity of smooth muscle by means of thesucrose gap. Proc. I Vth International Symposium on Gatrointestinal Motility (Banff, Canada),pp. 409-425. Vancouver: Mitchell Press.

SZURSZEWSKI, J. H. (1975). Mechanism of action of pentagastrin and acetylcholine on the longi-tudinal muscle of the canine antrum. J. Physiol. 252, 335-361.

TALBOT, S. A., LILIENTHAL, J. L., BESER, J. J. & REYNOLDS, L. W. (1951). A wide rangemechano-electronic transducer for physiological applications. Rev. Scient. Instrum. 22, 233-236.

TAYLOR, I., SMALLWOOD, R. & DUTIE, H. L. (1973). Myoelectrical activity in the rectosigmoidin man. Proc. IVth International Symposium on Gastrointestinal Motility (Banif, Canada),pp. 109-118. Vancouver: Mitchell Press.

USTACH, J., TOBON, F., HAMBRECHT, T., BASS, D. & SchtusTER, M. (1970). Electrophysiologicalaspects of human sphincter function. J. clin. Invest. 49, 41-48.

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Electrical activity from smooth muscle of the anal sphincteric area of