A comparative study of structure and function of the longitudinal muscle of the anal canal and the internal anal sphincter in pigs.
OBJECTIVE
This study aims to compare the physiology of the longitudinal muscle of the anal canal with the internal anal sphincter in pigs.


METHODS
Histology and in vitro studies were performed to compare the effect of neural responses induced by electric stimulation and through nicotinic, purinergic, and serotoninergic receptors.


RESULTS
The longitudinal muscle and the internal anal sphincter are constituted exclusively by smooth muscle. Strips from the internal anal sphincter a) developed myogenic tone; b) responded to electric stimulation with an "on" relaxation antagonized by nitric oxide synthase inhibitors and purinergic P2Y1 antagonists, and with an "off" contraction antagonized by atropine and phentolamine; and c) responded to stimulation of nicotinic receptors with a relaxation antagonized by nitrergic and purinergic P2Y1 antagonists, responded to stimulation of serotoninergic 5-hydroxytryptamine 3 receptors with a contraction, and relaxed to carbachol and purinergic P2X agonists. Strips from the longitudinal muscle a) did not develop tone, b) responded to electric stimulation with an "on" contraction antagonized by atropine, and c) did not respond to stimulation of nicotinic or serotoninergic 5-hydroxytryptamine 3 receptors, and carbachol and purinergic P2X agonists induced a contraction.


CONCLUSIONS
The motility of the internal anal sphincter includes myogenic tone, relaxation mediated by nitric oxide and purinergic P2Y1 receptors, and contraction mediated by cholinergic motor neurons and sympathetic fibers. The motility of the longitudinal muscle is limited to a contraction mediated by cholinergic neurons, suggesting that longitudinal muscle contracts during relaxation of the internal sphincter, shortening the anal canal. Nicotinic, muscarinic, and serotoninergic receptors might be therapeutic targets for anal motor disorders.
Opazo
Alvaro
A
Department of Surgery, Hospital de Mataró, Universitat Autònoma de Barcelona, 08304, Mataró, Spain.
Lecea
Begoña
B
Admella
Carme
C
Fantova
Maria José
MJ
Jiménez
Marcel
M
Martí-Ragué
Joan
J
Clavé
Pere
P
D000244:Adenosine Diphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D001003:Anal Canal / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D004558:Electric Stimulation; D008297:Male; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide / Q000494:pharmacology; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000502:physiology; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology; D011985:Receptors, Serotonin / Q000187:drug effects / Q000502:physiology; D013552:Swine; D013873:Thionucleotides / Q000494:pharmacology
D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D011985:Receptors, Serotonin; D013873:Thionucleotides; D009599:Nitroprusside; C030812:adenosine 5'-O-(2-thiodiphosphate); D000244:Adenosine Diphosphate; D001285:Atropine; D002217:Carbachol; D019001:Nitric Oxide Synthase; D010646:Phentolamine