Mechanism of action of pentagastrin and acetylcholine on the longitudinal muscle of the canine antrum.

Szurszewski, Joseph H.

doi:10.1113/jphysiol.1975.sp011147

Cited by 80 publications

(54 citation statements)

References 24 publications

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“…This increase in the size of the plateau potential was associated with an increase in the force of the phasic, antral contraction. This association of an increase in the size of the plateau potential with an increase in the force of contraction has been seen previously in response to exogenous acetylcholine (Szurszewski, 1975). In the fundus the mean resting potential is -52 mV and the mechanical threshold is approximately -52 mV.…”

Section: Resultssupporting

confidence: 82%

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The electrical basis for contraction and relaxation in canine fundal smooth muscle

Morgan¹,

Muir

Szurszewski³

1981

The Journal of Physiology

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SUMMARY1. Mechanical and intracellular electrical activities were recorded simultaneously from canine fundal and antral smooth muscle preparations.2. Most fundal preparations displayed no spontaneous electrical or mechanical activity. The tissue had a space constant of 1.5 mm and a time constant of 189 msec and showed outward rectification in response to depolarizing current. 3. Transmural nerve stimulation offundal preparations demonstrated the presence ofcholinergic excitatory and non-cholinergic, non-adrenergic inhibitory neural inputs to the tissue. The cholinergic nerve response consisted ofa small, graded depolarization accompanied by a slow graded contraction; the inhibitory nerve response consisted of a graded hyperpolarization accompanied by a slow relaxation.4. The excitatory fundal nerve response was abolished or greatly diminished by D600 and Mn2+. D600 and Mn2+ also decreased basal tone. The inhibitory nerve response was unaffected by either agent. 5. The excitatory nerve response in the fundus was contrasted with the excitatory nerve response in the antrum. In the fundus, stimulation of cholinergic motor nerves produced a depolarization which always produced a contraction. In the antrum, stimulation of cholinergic motor nerves between action potentials produced graded depolarizations of antral cells; however, there were no associated contractions. Stimulation of cholinergic motor nerves during spontaneous action potentials increased the amplitude and duration of the plateau phase of the action potential; this was associated with an augmentation of the spontaneous contractions.6. Voltage-tension curves were determined for antral and fundal preparations using K+ depolarization as a means of controlling membrane potential. Antral preparations displayed a voltage threshold for contraction at a membrane potential approximately 30 mV positive to the resting potential. In contrast, fundal resting potentials were at or more positive than their voltage thresholds.7. These differences in electromechanical coupling provide an explanation for the marked differences in the responses of fundal and antral smooth muscles to nerve stimulation and account for their physiologic function in vivo.

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Section: Resultssupporting

confidence: 82%

“…Muscles were stretched by 0-5-1-0 mm increments until the contraction caused by acetylcholine (ACh 10-6 M) was maximum. The passive tension at which the contraction was maximum was maintained throughout the experiment (Szurszewski, 1975). At this optimal length, 9000 of the preparations showed no spontaneous electrical or mechanical activity.…”

Section: Resultsmentioning

confidence: 98%

The electrical basis for contraction and relaxation in canine fundal smooth muscle

Morgan¹,

Muir

Szurszewski³

1981

The Journal of Physiology

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“…34). It is of interest, however, that acetylcholine has long been known to cause a striking prolongation and elevation of action potentials in guinea-pig ileum (1) and canine gastric antrum (35) (15,16,43,44). In the present study, neither GTP nor other metabolically active cytosolic substances were present in the patch pipette.…”

Section: Discussionmentioning

confidence: 59%

Acetylcholine increases voltage-activated Ca2+ current in freshly dissociated smooth muscle cells.

Vivaudou¹,

Walsh²,

Singer³

1987

Proc. Natl. Acad. Sci. U.S.A.

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The regulation of voltage-activated Ca2+ current by acetylcholine was studied in single freshly dissociated smooth muscle cells from the stomach of the toad Bufo marinus by using the tight-seal whole-cell recording technique. Ca2+ currents were elicited by positive-going command pulses from a holding level near -80 mV in the presence of internal Cs' to block outward KV currents. Ca2+ current was greatest in magnitude at command potentials near 10 mV. At such command potentials, acetylcholine increased the magnitude of the inward current and slowed its decay. The effects of acetylcholine were seen in the absence of external Na' or with low Cl (aspartate replacement) in the bathing solution and could be mimicked by muscarine. The peak of the current-voltage relationship for the Ca2+ current was not discernibly shifted along the voltage axis by acetylcholine. These results demonstrate that activation of muscarinic receptors not only Acetylcholine, acting directly on muscarinic receptors in the smooth muscle cell membrane, causes depolarization, action potential generation, and, ultimately, contraction in a wide variety of smooth muscle types (1). To investigate the mechanism of acetylcholine action, we have used a preparation of freshly dissociated smooth muscle cells from the stomach of the toad Bufo marinus, where acetylcholine has been shown to exert an excitatory action (2-4). These cells have the advantage that their electrical activity has been extensively characterized by current-clamp (5, 6), voltageclamp (7,8), and patch-clamp (9) techniques.Recently, we demonstrated that one mechanism of muscarinic action on these smooth muscle cells is suppression of K+ current (2). This current bears a general similarity to the muscarine-sensitive K+ current, designated M-current, which was first described in sympathetic neurons (10)(11)(12) Series resistance compensation proved to be unnecessary since it was calculated that maximum inward currents produced a 2-to 5-mV error due to the series resistance and that the increase in current induced by acetylcholine or muscarine produced a 0.5-to 2-mV error. In what is referred to below as the standard voltage-clamp paradigm, the membrane potential was held at -78 mV for 6 sec, with alternating 3-sec command pulses to -98 and +9 mV, providing a total recovery time of 15 sec for the inward current. Deviations from this paradigm are indicated.Current and voltage signals were stored using an FM tape recorder, digitized later at a rate of 1 kHz after filtering (8-pole Bessel filter, 300-Hz cut-off) and analyzed with a PDP-11/73 computer system (Indec Systems). Traces shown in the figures were further filtered by using a digital gaussian filter (23), and in these cases the filter cut-off and effective sampling frequency are specified in the figure legends. Capacitive transients were blanked for reasons of clarity. Subtraction of the capacitive transients and leakage current with scaled averages of small (10-20 mV) hyperpolarizing pulses demonstrated that the inward curren...

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“…18 Acetylcholine (ACh), the dominant excitatory neurotransmitter in the GI tract, is released from enteric excitatory motor neurons. 1 ACh has ionotropic and chronotropic effects on gastric muscles, 19,20 and may increase slow wave amplitude and frequency and the fidelity of propagation in the post-prandial state. After release from neurons, ACh is efficiently metabolized by cholinesterases (AChE and BChE).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Gastric Electrical and Mechanical Activity by Cholinesterases in Mice

Worth

Forrest

Peri

et al. 2015

J Neurogastroenterol Motil

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Background/AimsGastric peristalsis begins in the orad corpus and propagates to the pylorus. Directionality of peristalsis depends upon orderly generation and propagation of electrical slow waves and a frequency gradient between proximal and distal pacemakers. We sought to understand how chronotropic agonists affect coupling between corpus and antrum. Methods Electrophysiological and imaging techniques were used to investigate regulation of gastric slow wave frequency by muscarinic agonists in mice. We also investigated the expression and role of cholinesterases in regulating slow wave frequency and motor patterns in the stomach. Results Both acetycholinesterase (Ache) and butyrylcholine esterase (Bche) are expressed in gastric muscles and AChE is localized to varicose processes of motor neurons. Inhibition of AChE in the absence of stimulation increased slow wave frequency in corpus and throughout muscle strips containing corpus and antrum. CCh caused depolarization and increased slow wave frequency. Stimulation of cholinergic neurons increased slow wave frequency but did not cause depolarization. Neostigmine (1 M) increased slow wave frequency, but uncoupling between corpus and antrum was not detected. Motility mapping of contractile activity in gastric muscles showed similar effects of enteric nerve stimulation on the frequency and propagation of slow waves, but neostigmine (＞ 1 M) caused aberrant contractile frequency and propagation and ectopic pacemaking. Conclusions Our data show that slow wave uncoupling is difficult to assess with electrical recording from a single or double sites and suggest that efficient metabolism of ACh released from motor neurons is an extremely important regulator of slow wave frequency and propagation and gastric motility patterns.

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Mechanism of action of pentagastrin and acetylcholine on the longitudinal muscle of the canine antrum.

Cited by 80 publications

References 24 publications

The electrical basis for contraction and relaxation in canine fundal smooth muscle

The electrical basis for contraction and relaxation in canine fundal smooth muscle

Acetylcholine increases voltage-activated Ca2+ current in freshly dissociated smooth muscle cells.

Regulation of Gastric Electrical and Mechanical Activity by Cholinesterases in Mice

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