Influence of sacral nerves on the internal anal sphincter of the opossum

The purpose of the present studies is to 1) compare the effects of stimulation of different sacral nerves (S1-S5) on internal anal sphincter (IAS) pressures and 2) examine the nature of synaptic transmission in the sacral inhibitory pathway to the IAS. Pressures from the IAS of alpha-chloralose-anesthetized opossums were recorded using a low-compliance continuously perfused catheter assembly. Electrical stimulation of the third and fourth sacral nerves (S3 and S4) caused frequency-dependent IAS relaxation, whereas stimulation of other sacral nerves was without significant effect on the IAS. Relaxation of the IAS in response to S4 stimulation was not significantly modified by atropine, pirenzepine dihydrochloride, hexamethonium chloride, or adrenergic antagonists. However, a combination of either atropine and hexamethonium or pirenzepine and hexamethonium caused a significant antagonism of sacral nerve-stimulated relaxation without modifying the inhibitory responses of local transmural nerve stimulation and isoproterenol. From these studies we conclude that 1) in the opossum the sacral nerves primarily exert inhibitory influences on the IAS and 2) the sacral inhibitory pathway involves the release of acetylcholine from preganglionic fibers, which in turn causes the activation of both muscarinic (M1) and nicotinic receptors on postganglionic, noncholinergic, nonadrenergic inhibitory neurons.

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Release of nitric oxide by activation of nonadrenergic noncholinergic neurons of internal anal sphincter

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1993.264.1.g7 ◽

1993 ◽

Vol 264 (1) ◽

pp. G7-G12 ◽

Cited By ~ 5

Author(s):

S. Chakder ◽

S. Rattan

Keyword(s):

Nitric Oxide ◽

Smooth Muscle ◽

Anal Sphincter ◽

Internal Anal Sphincter ◽

Smooth Muscles ◽

Electrical Field Stimulation ◽

Didelphis Virginiana ◽

Inhibitory Neurons ◽

No Release ◽

Stimulation Of

The purpose of the present study was to investigate the direct release of nitric oxide (NO) in response to the stimulation of nonadrenergic noncholinergic (NANC) nerves. The studies were performed on isolated smooth muscle strips of the opossum (Didelphis virginiana) internal anal sphincter (IAS). Electrical field stimulation (EFS) using the appropriate parameters caused a frequency-dependent fall in the resting tone of the IAS. The release of NO was measured directly by the chemiluminescence method. The stimulation of NANC neurons by EFS and the nicotinic stimulant 1,1-dimethyl-4-phenylpiperazinium (DMPP) caused IAS relaxation with an accompanying release of NO. The release of NO and the fall in the resting tension of IAS in response to lower frequencies of EFS and DMPP were abolished by pretreatment of the smooth muscles with the neurotoxin tetrodotoxin and the NO-synthase inhibitor NG-nitro-L-arginine (L-NNA). The obliteration of the release of NO and the IAS relaxation in the presence of L-NNA reversed to control levels by the addition of the NO precursor L-arginine. The effect of L-NNA and L-arginine on NO release and IAS relaxation was stereoselective, since D-NNA and D-arginine had no significant effect. Vasoactive intestinal polypeptide also caused release of NO from IAS smooth muscle strips, which was abolished by L-NNA. However, isoproterenol and atrial natriuretic factor caused IAS relaxation without any increase in NO release. In conclusion, these studies demonstrate the direct release of NO in response to the stimulation of NANC inhibitory neurons of the gut.

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Influence of purinoceptors' agonists and antagonists on opossum internal anal sphincter

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.255.3.g389 ◽

1988 ◽

Vol 255 (3) ◽

pp. G389-G394 ◽

Cited By ~ 3

Author(s):

S. Rattan ◽

R. Shah

Keyword(s):

Anal Sphincter ◽

Internal Anal Sphincter ◽

Inhibitory Effect ◽

Inhibitory Response ◽

Rectal Balloon ◽

Balloon Distension ◽

Before And After ◽

High Doses ◽

Alpha Chloralose ◽

Dose Dependent

Studies were performed in alpha-chloralose-anesthetized and pancuronium-treated opossums. Resting internal anal sphincter pressures (IASP) were monitored using low-compliant continuously perfused catheters. P1 and P2 purinoceptor agonists, adenosine and ATP, respectively, administered close intra-arterially, caused dose-dependent decreases in the IASP. The inhibitory effect of these agonists on the IASP was tetrodotoxin resistant. Rectal balloon distension (RD) (which mimics the rectoanal inhibitory reflex) caused volume-dependent IAS relaxation. Electrical stimulation of the sacral nerve (SNS) also produced frequency-dependent decreases in IASP. The inhibitory response to adenosine (P1 purinoceptor agonist), ATP (P2 purinoceptor agonist), RD, and SNS on the internal anal sphincter (IAS) was examined before and after 8-phenyltheophylline (P1 purinoceptor antagonist) and alpha,beta-methylene ATP (P2 purinoceptor antagonist that irreversibly binds and desensitizes P2 purinoceptor). P1 and P2 purinoceptor antagonists produced selective antagonism of the inhibitory responses on the IAS of their respective agonists only. Furthermore, high doses of adenosine and ATP produced desensitization and block of their own actions only. The purinoceptors' antagonists, and the desensitization of purinoceptors by high doses of adenosine and ATP, failed to modify the fall in IASP in response to RD or SNS. From these studies we conclude that distinct inhibitory P1 and P2 purinoceptors are present on the IAS smooth muscle. However, these inhibitory purinoceptors may not be responsible for the rectoanal reflex-mediated IAS relaxation.

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Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.5.g709 ◽

1992 ◽

Vol 263 (5) ◽

pp. G709-G718 ◽

Cited By ~ 13

Author(s):

M. Schemann ◽

D. Grundy

Keyword(s):

Nicotinic Receptors ◽

Vagal Stimulation ◽

Enteric Neurons ◽

Command Neurons ◽

Myenteric Neurons ◽

Release Of Acetylcholine ◽

Vagal Innervation ◽

Guinea Pig Stomach ◽

Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

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The response of the internal anal sphincter in man to stimulation of the presacral nerve

The American Journal of Digestive Diseases ◽

10.1007/bf02233661 ◽

1968 ◽

Vol 13 (5) ◽

pp. 421-427 ◽

Cited By ~ 32

Author(s):

J. J. Shepherd ◽

P. G. Wright

Keyword(s):

Anal Sphincter ◽

Internal Anal Sphincter ◽

Stimulation Of

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Genesis of anal canal pressures in the opossum

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.6.g765 ◽

1986 ◽

Vol 251 (6) ◽

pp. G765-G771 ◽

Cited By ~ 26

Author(s):

P. J. Culver ◽

S. Rattan

Keyword(s):

Anal Canal ◽

Anal Sphincter ◽

Internal Anal Sphincter ◽

External Anal Sphincter ◽

Sphincter Pressure ◽

Electromyographic Activity ◽

Sphincter Muscle ◽

Anal Sphincter Muscle ◽

Adrenergic Antagonist ◽

Alpha Chloralose

The purpose of the present investigation was to examine the role of the internal and external anal sphincters in the maintenance of resting pressures in the anal canal. The studies were performed in opossums anesthetized with alpha-chloralose. The radial and axial pressures in the anal canal were monitored using a continuously perfused catheter assembly. Electromyography of the external anal sphincter was monitored using bipolar tungsten hook electrodes. To examine the contribution of the external anal sphincter and surrounding skeletal muscle to the resting tone in the anal canal, pancuronium bromide was administered in a dose that abolished the electromyographic activity of the external anal sphincter muscle. The abolition of external anal sphincter activity did not modify the peak anal canal pressures, suggesting that these pressures are due to the internal anal sphincter. The alpha-adrenergic antagonist, phentolamine, did not modify the anal canal pressure, suggesting that basal internal anal sphincter pressure is not due to tonic adrenergic activity. Tetrodotoxin in a dose that produced obliteration of the anorectal reflex causing anal sphincter relaxation did not produce any change in the peak anal canal pressures. These studies show that the resting pressures in the anal canal of opossums are due to myogenic properties of the internal anal sphincter.

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