The relationship between propagated contractions and pseudoaffective changes in blood pressure in response to intestinal distension.
We investigated the relationship between changes in small intestinal motility and changes in blood pressure and heart rate in response to intestinal distension. Rats were maintained under stable anaesthesia with alpha-chloralose, and jejunal motility, blood pressure and heart rate were recorded. Pressure changes during propagated contractions of the circular muscle were recorded in the jejunum when the intraluminal pressure was maintained at 10 mmHg. Raising the pressure in 10 mmHg increments from 10 mmHg to 40 mmHg increased the frequency of propagated contractions from 0.30 +/- 0.06 min-1 (mean +/- SEM) to 1.29 +/- 0.09 per min. In contrast, amplitudes of contractions above baseline pressure decreased from 19.5 +/- 0.6 mmHg to 7.8 +/- 0.5 mmHg. Simultaneously, blood pressure and heart rate were both increased. Pretreatment of rats with capsaicin, or severing the mesenteric nerves acutely, prevented these cardiovascular responses, but did not influence the changes in propagated activity caused by distension. Propagated contractions were blocked by hexamethonium (10 mg kg-1, intravenously [i.v.]) and by local application of 2% lidocaine, but propulsion was unchanged by hyoscine (1 mg kg-1, i.v.). Phentolamine (1 mg kg-1, i.v.) increased the frequency of propagated contractions. The methods described in this work allow the effects of drugs on intrinsic intestinal reflexes to be distinguished from their effects on extra-intestinal, pseudoaffective reflexes. In addition, unlike other experiments using anaesthetized rats, blood pressure increased in response to distension, as it does in mammals that are not anaesthetized. The experiments demonstrate that the neural pathways for propagated contractions that rely on intrinsic nerve circuits, including intrinsic primary afferent neurones, and the neural pathways for extrinsic reflexes that signal pain or discomfort in the intestine, which involve capsaicin-sensitive spinal afferent neurones, are independent.
Timar-Peregrin
A
A
Department of Anatomy and Cell Biology and Centre for Neuroscience, The University of Melbourne, Victoria, Australia. peregrin@unimelb.edu.au
Kumano
K
K
Khalil
Z
Z
Sanger
G J
GJ
Furness
J B
JB
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000339:Affect / Q000502:physiology*; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002211:Capsaicin / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D007422:Intestines / Q000187:drug effects / Q000502:physiology*; D008012:Lidocaine / Q000494:pharmacology; D008643:Mesentery / Q000294:innervation; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology / Q000523:psychology; D010812:Physical Stimulation; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000187:drug effects / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; D000779:Anesthetics, Local; D018727:Muscarinic Antagonists; D018733:Nicotinic Antagonists; D008012:Lidocaine; D002211:Capsaicin