The effects of antiinflammatory steroids on the response of the guinea-pig isolated ileum to acetylcholine, histamine, nicotine, 5-hydroxytryptamine and electrical stimulation

1979 ◽  
Vol 309 (2) ◽  
pp. 191-195 ◽  
Author(s):  
Jean-Pierre Famaey ◽  
Jeanine Fontaine ◽  
Isabelle Seaman ◽  
Jean Reuse
1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall

1983 ◽  
Vol 245 (3) ◽  
pp. H475-H480
Author(s):  
J. G. Dobson

Isolated guinea pig atria stimulated to contract isometrically were used to determine whether adenosine at a concentration that does not cause a direct depressant effect on peak contractile force, rate of force development, and rate of relaxation was capable of influencing the elevation in these contractile parameters caused by an increase in preload, paired electrical stimulation, an increase in contraction frequency, and catecholamine stimulation in K+-depolarized and nondepolarized atrial muscle. Adenosine had no effect on the contractile parameters that were enhanced by an increase in preload or paired electrical stimulation. The nucleoside reduced the increases in the contractile parameters produced by isoproterenol stimulation, an increase in contraction frequency, and isoproterenol-induced contractions in depolarized atria. All adenosine reductions were inhibited by theophylline, an antagonist of adenosine actions. The adenosine reduction of the elevated contractile parameters caused by increasing contraction frequency was not prevented by atropine (a muscarinic antagonist) or propranolol (a beta-adrenergic blocking agent). These results suggest that adenosine at a concentration that does not produce direct negative inotropic responses is capable of attenuating the elevation in contractility elicited by catecholamine stimulation, an increase in contraction frequency, and catecholamine-induced contractions in depolarized atria. However, the reduction by adenosine of the contractile responses elicited by an increase in contraction frequency appears to be independent of catecholamines.


1979 ◽  
Vol 237 (2) ◽  
pp. E198
Author(s):  
D L Vermillion ◽  
J P Gillespie ◽  
A R Cooke ◽  
J D Wood

Intrinsic inhibitory neurons to guinea pig taenia coli and small bowel circular muscle were activated by transmural electrical stimulation, and the postinhibitory contractile response of the muscle was utilized to evaluate whether or not the neuronal action of 5-hydroxytryptamine (5HT) was associated with the inhibitory neurons. The postinhibitory contractile responses of the small intestinal circular muscle were unaffected by 5HT. The 5HT antagonist methysergide also did not affect the poststimulus contractile response of the circular muscle. The amplitude and area under the contractile curve of the poststimulus contractile response of the taenia coli were reduced and the amplitude of the relaxation response to electrical stimulation was increased in one-half of the preparations after application of 5HT. Methysergide did not alter the poststimulus contractile response of the taenia coli. 5HT is implicated as a neurotransmitter substance for slow synaptic excitation within the enteric nervous system of the guinea pig small intestine; however, the 5HT synapses do not appear to be present on the "purinergic" inhibitory neurons nor on neurons that synaptically influence the inhibitory neurons.


1983 ◽  
Vol 245 (6) ◽  
pp. G745-G750 ◽  
Author(s):  
H. J. Cooke ◽  
K. Shonnard ◽  
G. Highison ◽  
J. D. Wood

Scorpion venom (Leiurus quinquestriatus), a substance that evokes neurotransmitter release by depolarizing neurons, was used to activate enteric neurons in short-circuited guinea pig ileum. Scorpion venom increased transmural potential difference and short-circuit current, and this response was similar to the increase that occurred after electrical stimulation of enteric neurons. The stimulus- or venom-evoked response in short-circuit current was abolished by tetrodotoxin. Atropine reduced by 47% the increments in short-circuit current produced by either electrical stimulation or venom. Scorpion venom increased active chloride secretion in short-circuited guinea pig ileal mucosa but had no significant effect on active sodium absorption, residual flux, or total tissue conductance. No morphological changes in transmission electron micrographs of ileal mucosa treated with scorpion venom were evident compared with controls. Alanine caused an increase in short-circuit current in venom-treated tissue that was similar to control values. These results show that scorpion venom mimics the mucosal effects of electrical activation of enteric neurons. These results suggest that a significant component of both scorpion venom action and the response to electrical field stimulation is mediated by neural release of acetylcholine, which activates epithelial muscarinic receptors.


2014 ◽  
Vol 307 (7) ◽  
pp. G719-G731 ◽  
Author(s):  
Guo-Du Wang ◽  
Xi-Yu Wang ◽  
Sumei Liu ◽  
Meihua Qu ◽  
Yun Xia ◽  
...  

Mast cells express the substance P (SP) neurokinin 1 receptor and the calcitonin gene-related peptide (CGRP) receptor in guinea pig and human small intestine. Enzyme-linked immunoassay showed that activation of intramural afferents by antidromic electrical stimulation or by capsaicin released SP and CGRP from human and guinea pig intestinal segments. Electrical stimulation of the afferents evoked slow excitatory postsynaptic potentials (EPSPs) in the enteric nervous system. The slow EPSPs were mediated by tachykinin neurokinin 1 and CGRP receptors. Capsaicin evoked slow EPSP-like responses that were suppressed by antagonists for protease-activated receptor 2. Afferent stimulation evoked slow EPSP-like excitation that was suppressed by mast cell-stabilizing drugs. Histamine and mast cell protease II were released by 1) exposure to SP or CGRP, 2) capsaicin, 3) compound 48/80, 4) elevation of mast cell Ca2+ by ionophore A23187, and 5) antidromic electrical stimulation of afferents. The mast cell stabilizers cromolyn and doxantrazole suppressed release of protease II and histamine when evoked by SP, CGRP, capsaicin, A23187, electrical stimulation of afferents, or compound 48/80. Neural blockade by tetrodotoxin prevented mast cell protease II release in response to antidromic electrical stimulation of mesenteric afferents. The results support a hypothesis that afferent innervation of enteric mast cells releases histamine and mast cell protease II, both of which are known to act in a diffuse paracrine manner to influence the behavior of enteric nervous system neurons and to elevate the sensitivity of spinal afferent terminals.


1982 ◽  
Vol 91 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Ben M. Clopton ◽  
Martha M. Bosma

Electrical stimulation of afferent auditory elements through electrodes placed in the middle ear was investigated in acute guinea pig preparations. Thresholds for auditory activation were current-dependent for low frequencies (<1 kHz) and charge-dependent at higher frequencies. Threshold currents were 3–5 times those for intracochlear stimulation. Mechanisms of activation were examined with removal of cochlear fluids and injection of neomycin, Xylocaine, saline, and artificial perilymph with different calcium concentrations. Neurons of the spiral ganglion are indicated as mediators of this stimulation.


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