Antigen depolarizes guinea pig bronchial parasympathetic ganglion neurons by activation of histamine H1 receptors

1995 ◽  
Vol 268 (6) ◽  
pp. L879-L884 ◽  
Author(s):  
A. C. Myers ◽  
B. J. Undem
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
High Titer ◽  
Membrane Resistance ◽  
Dependent Manner ◽  
Immediate Hypersensitivity ◽  
Concentration Dependent Manner ◽  
Parasympathetic Ganglion ◽  
Histamine H1 Receptors ◽  
Ganglion Neurons

Studies were carried out to evaluate the mechanism by which neurotransmission through airway parasympathetic ganglia may be modulated during immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-ovalbumin antibodies. Intracellular recordings were obtained from intrinsic parasympathetic ganglion neurons from the right mainstem bronchus in vitro. Ovalbumin (10 micrograms/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial ganglion neurons from passively sensitized guinea pigs. Histamine mimicked the depolarizing effect of ovalbumin in a concentration-dependent manner (0.1–10 microM) and caused a transient increase and decrease in membrane resistance. Pyrilamine, a histamine H1-receptor antagonist, inhibited the histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking histamine H2 and H3 receptors did not inhibit histamine-induced depolarization. Pyrilamine also reduced the antigen-induced depolarization of ganglion neurons, demonstrating a role for histamine H1 receptors in this response. The data provide evidence that the antigen-induced depolarization of airway ganglion neurons is secondary to an antigen-antibody interaction on intrinsic mast cells and the consequential effect of histamine on H1 receptors. These studies demonstrate that histamine released during an immediate hypersensitivity reaction has direct effects on airway parasympathetic nerves.

Ba2+, TEA+, and quinine effects on apical membrane K+ conductance and maxi K+ channels in gallbladder epithelium

1990 ◽  
Vol 259 (1) ◽  
pp. C56-C68 ◽  
Author(s):  
Y. Segal ◽  
L. Reuss
Keyword(s):  
Apical Membrane ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
K Channel ◽  
Dependent Manner ◽  
Gallbladder Epithelium ◽  
Concentration Dependent Manner ◽  
K Channels ◽  
Voltage Dependent ◽  
Channel Currents

The apical membrane of Necturus gallbladder epithelium contains a voltage-activated K+ conductance [Ga(V)]. Large-conductance (maxi) K+ channels underlie Ga(V) and account for 17% of the membrane conductance (Ga) under control conditions. We examined the Ba2+, tetraethylammonium (TEA+), and quinine sensitivities of Ga and single maxi K+ channels. Mucosal Ba2+ addition decreased resting Ga in a concentration-dependent manner (65% block at 5 mM) and decreased Ga(V) in a concentration- and voltage-dependent manner. Mucosal TEA+ addition also decreased control Ga (60% reduction at 5 mM). TEA+ block of Ga(V) was more potent and less voltage dependent that Ba2+ block. Maxi K+ channels were blocked by external Ba2+ at millimolar levels and by external TEA+ at submillimolar levels. At 0.3 mM, quinine (mucosal addition) hyperpolarized the cell membranes by 6 mV and reduced the fractional apical membrane resistance by 50%, suggesting activation of an apical membrane K+ conductance. At 1 mM, quinine both activated and blocked K(+)-conductive pathways. Quinine blocked maxi K+ channel currents at submillimolar concentrations. We conclude that 1) Ba2+ and TEA+ block maxi K+ channels and other K+ channels underlying resting Ga; 2) parallels between the Ba2+ and TEA+ sensitivities of Ga(V) and maxi K+ channels support a role for these channels in Ga(V); and 3) quinine has multiple effects on K(+)-conductive pathways in gallbladder epithelium, which are only partially explained by block of apical membrane maxi K+ channels.

Guinea pig visceral C-fiber neurons are diverse with respect to the K+ currents involved in action-potential repolarization

1994 ◽  
Vol 71 (2) ◽  
pp. 561-574 ◽  
Author(s):  
E. P. Christian ◽  
J. Togo ◽  
K. E. Naper
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Outward Current ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Whole Cell ◽  
C Fiber ◽  
K Current ◽  
Action Potential Repolarization

1. Intracellular recordings were made from C-fiber neurons identified by antidromic conduction velocity in intact guinea pig nodose ganglia maintained in vitro, and whole-cell patch clamp recordings were made from dissociated guinea pig nodose neurons to investigate the contribution of various K+ conductances to action-potential repolarization. 2. The repolarizing phase of the intracellularly recorded action potential was prolonged in a concentration-dependent manner by charybdotoxin (Chtx; EC50 = 39 nM) or iberiatoxin (Ibtx; EC50 = 48 nM) in a subpopulation of 16/36 C-fiber neurons. In a subset of these experiments, removal of extracellular Ca2+ reversibly prolonged action-potential duration (APD) in the same 4/9 intracellularly recorded C-fiber neurons affected by Chtx (> or = 100 nM). These convergent results support that a Ca(2+)-activated K+ current (IC) contributes to action-potential repolarization in a restricted subpopulation of C-fiber neurons. 3. Tetraethylammonium (TEA; 1-10 mM) increased APD considerably further in the presence of 100-250 nM Chtx or Ibtx, or in nominally Ca(2+)-free superfusate in 14/14 intracellularly recorded C-fiber neurons. TEA affected APD similarly in subpopulations of neurons with and without IC, suggesting that a voltage-dependent K+ current (IK) contributes significantly to action-potential repolarization in most nodose C-fiber neurons. 4. Substitution of Mn2+ for Ca2+ reduced outward whole-cell currents elicited by voltage command steps positive to -30 mV (2-25 ms) in a subpopulation of 21/36 dissociated nodose neurons, supporting the heterogeneous expression of IC. The kinetics of outward tail current relaxations (tau s of 1.5-2 ms) measured at the return of 2-3 ms depolarizing steps to -40 mV were indistinguishable in neurons with and without IC, precluding a separation of the nodose IC and IK by a difference in deactivation rates. 5. Chtx (10-250 nM) reduced in a subpopulation of 3/8 C-fiber neurons the total outward current elicited by voltage steps depolarized to -30 mV in single microelectrode voltage-clamp recordings. TEA (5-10 mM) further reduced outward current in the presence of 100-250 nM Chtx in all eight experiments. The Chtx-sensitive current was taken to represent IC, and the TEA-sensitive current, the IK component contributing to action-potential repolarization. 6. Rapidly inactivating current (IA) was implicated in action-potential repolarization in a subpopulation of intracellularly recorded C-fiber neurons. In 4/7 neurons, incremented hyperpolarizing prepulses negative to -50 mV progressively shortened APD.(ABSTRACT TRUNCATED AT 400 WORDS)

Mg2+ Inhibition of ATP-Activated Current in Rat Nodose Ganglion Neurons: Evidence That Mg2+ Decreases the Agonist Affinity of the Receptor

1997 ◽  
Vol 77 (6) ◽  
pp. 3391-3395 ◽  
Author(s):  
Chaoying Li ◽  
Robert W. Peoples ◽  
Forrest F. Weight
Keyword(s):  
Nodose Ganglion ◽  
Dependent Manner ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
Agonist Affinity ◽  
Nodose Ganglion Neurons ◽  
Whole Cell Patch Clamp ◽  
Activation Rate ◽  
The Right ◽  
Ganglion Neurons

Li, Chaoying, Robert W. Peoples, and Forrest F. Weight. Mg2+ inhibition of ATP-activated current in rat nodose ganglion neurons: evidence that Mg2+ decreases the agonist affinity of the receptor. J. Neurophysiol. 77: 3391–3395, 1997. The effect of Mg2+ on ATP-activated current in rat nodose ganglion neurons was investigated with the use of the whole cell patch-clamp technique. Mg2+ decreased the amplitude of ATP-activated current in a concentration-dependent manner over the concentration range of 0.25–8 mM, with a 50% inhibitory concentration value of 1.5 mM for current activated by 10 μM ATP. Mg2+ shifted the ATP concentration-response curve to the right in a parallel manner, increasing the 50% effective concentration value for ATP from 9.2 μM in the absence of added Mg2+ to 25 μM in the presence of 1 mM Mg2+. Mg2+ increased the deactivation rate of ATP-activated current without changing its activation rate. The observations are consistent with an action of Mg2+ to inhibit ATP-gated ion channel function by decreasing the affinity of the agonist binding site on these receptors.

Effect of bradykinin on membrane properties of guinea pig bronchial parasympathetic ganglion neurons

2000 ◽  
Vol 278 (3) ◽  
pp. L485-L491 ◽  
Author(s):  
Radhika Kajekar ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Sensory Nerve ◽  
Input Resistance ◽  
Inhibitory Effect ◽  
Membrane Properties ◽  
Alternative Mechanism ◽  
Induced Membrane ◽  
Parasympathetic Ganglion ◽  
Hoe 140 ◽  
Ganglion Neurons

The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (∼70%) as HOE-140. However, neurokinin-1 and -3 receptor antagonists did not have similar inhibitory effects. The ability of bradykinin to directly alter active properties of parasympathetic ganglion neurons was also examined. Bradykinin (100 nM) significantly reduced the duration of the afterhyperpolarization (AHP) that followed four consecutive action potentials. The inhibitory effect of bradykinin on the AHP response was reversed by HOE-140 but not by indomethacin. These results indicate that bradykinin can stimulate airway parasympathetic ganglion neurons independent of sensory nerve activation and provide an alternative mechanism for regulating airway parasympathetic tone.

Vasodilation induced by substance P in guinea pig carotid arteries

1994 ◽  
Vol 266 (3) ◽  
pp. H1132-H1137
Author(s):  
G. Zhang ◽  
Y. Yamamoto ◽  
K. Miwa ◽  
H. Suzuki
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Carotid Arteries ◽  
Smooth Muscles ◽  
Peak Amplitude ◽  
Resting Potential ◽  
Dependent Manner ◽  
Similar Form ◽  
Concentration Dependent Manner ◽  
High K

In the guinea pig carotid artery with an intact endothelium, substance P (SP, 10(-10)-10(-7) M) relaxed the norepinephrine- (NE) contracted smooth muscles transiently, in a concentration-dependent manner. Acetylcholine (ACh, 10(-6) M) produced a sustained relaxation. SP and ACh also relaxed muscles contracted with high-K (29.6 mM) solution, with a similar form but with a reduced amplitude compared with findings in NE-contracted muscles. In the presence of nitroarginine (10(-5) M) and NE, the ACh-induced relaxation was transient, with a reduced amplitude, whereas the SP-induced relaxation was not significantly changed. In muscles contracted with high-K solution containing nitroarginine, neither SP nor ACh produced relaxation. SP (> 10(-11) M) transiently hyperpolarized the membrane, but only when this peptide was applied from the intimal side of the intact vessel, and the peak amplitude reached approximately 20 mV from the resting potential at 10(-8) M. ACh transiently hyperpolarized the membrane (the peak amplitude being approximately 10 mV), in both the adventitial and intimal applications. In high-K solution, neither SP nor ACh produced hyperpolarization. The amplitude of hyperpolarizations produced by SP did not significantly change in the presence of nitroarginine, oxyhemoglobin, or indomethacin. Thus, SP-induced relaxation seems to be produced mainly by endothelium-derived hyperpolarizing factor-induced hyperpolarization.

scholarly journals Phasic and Tonic Smooth Muscle Function of the Partially Obstructed Guinea Pig Intestine

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Jingbo Zhao ◽  
Donghua Liao ◽  
Jian Yang ◽  
Hans Gregersen
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Muscle Function ◽  
Circumferential Stress ◽  
Outer Diameter ◽  
Dependent Manner ◽  
Contraction Force ◽  
Jejunal Segment ◽  
Smooth Muscle Function

This study was to generate phasic and tonic stress-strain curves for evaluation of smooth muscle function in the obstructed guinea pig jejunum. Partial and sham obstruction of the jejunum in guinea pigs was created surgically, with guinea pigs not being operated on served as normal controls. The animals survived 2, 4, 7, and 14 days, respectively. The jejunal segment was distended to 10 cm H2O. The pressure and outer diameter changes were recorded. Passive conditions were obtained by using papaverine. Total phasic, tonic, and passive circumferential stress and strain were computed from the diameter and pressure data with reference to the zero-stress-state geometry. The active phasic and tonic stresses were defined as the total phasic and tonic stress minus the passive stress. The thickness of intestinal muscle layers increased in a time-dependent manner after obstruction. The amplitude of passive, total phasic, total tonic, active phasic, and active tonic circumferential stresses increased as function of strain 7 days after obstruction. However, when normalized to muscle layer thickness, the amplitude of active stresses did not differ among the groups. In conclusion, the long-term-obstructed intestine exhibits increased total smooth muscle contraction force. However, the contraction force per smooth muscle unit did not increase.

Molecular mechanism of doxorubicin-induced anticholinergic effect in guinea-pig atria

2000 ◽  
Vol 78 (6) ◽  
pp. 483-489 ◽  
Author(s):  
Yukio Hara ◽  
Kyosuke Temma ◽  
Zin Sekiya ◽  
Akihito Chugun ◽  
Hiroshi Kondo
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Acetylcholine Receptor ◽  
Action Potential Duration ◽  
Molecular Mechanisms ◽  
Muscarinic Acetylcholine Receptor ◽  
Anticholinergic Effect ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Muscarinic Acetylcholine

The molecular mechanisms of anticholinergic actions of doxorubicin were examined by electrophysiological methods in atria and myocytes isolated from guinea-pig heart. A direct anticholinergic action of doxorubicin was confirmed with antagonistic action on carbachol-induced negative inotropic effect in atria. Both carbachol and adenosine produced shortening of action potential duration in atria measured by a microelectrode method. Doxorubicin (10-100 µM) inhibited the carbachol-induced action potential shortening in a concentration-dependent manner. However, doxorubicin did not antagonize the shortening elicited by adenosine. The whole-cell voltage clamp technique was performed to induce the muscarinic acetylcholine-receptor-operated K+ current (IK.ACh) in atrial myocytes loaded with GTP or GTPgammaS, a nonhydrolysable analogue of GTP. Doxorubicin (1-100 µM) suppressed carbachol-induced IK.ACh in a concentration-dependent manner (IC50 = 5.6 µM). In contrast, doxorubicin (10 and 100 µM) suppressed neither adenosine-induced IK.ACh nor GTPgammaS-induced IK.ACh. These results indicate that doxorubicin produces a direct anticholinergic effect through the muscarinic receptors in atrial myocytes.Key words: action potential duration, anticholinergic action, atrial cell, doxorubicin, the muscarinic acetylcholine-receptor-operated K+ current.

Mechanism of the negative inotropic effect of adenosine in guinea pig atrial myocytes

1994 ◽  
Vol 267 (6) ◽  
pp. H2420-H2429
Author(s):  
D. Wang ◽  
L. Belardinelli
Keyword(s):  
Guinea Pig ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
Whole Cell Patch Clamp ◽  
K Current ◽  
Highly Correlated

The ionic basis of the negative inotropic effect of adenosine on guinea pig atrial myocytes was studied. Membrane potentials and currents were measured using a whole cell patch-clamp technique. The contractility was assessed by video quantitation of cell twitch amplitude. Adenosine shortened action potential duration [measured at 90% repolarization (APD90)] and decreased twitch amplitude in a concentration-dependent manner. The maximal effects of adenosine (100 microM) were to reduce APD90 from 102 +/- 14 to 34 +/- 8 ms (n = 11) and twitch amplitude from 4.3 +/- 0.9 to 1.5 +/- 0.4 microns (n = 8). The concentration of adenosine that caused one-half of the maximal reductions of twitch amplitude and of APD90 was 0.6 microM. Reductions in APD90 and in twitch amplitude were parallel and highly correlated (r = 0.98). Decreases in twitch amplitude by adenosine could be mimicked by application of voltage-clamp pulses with durations similar to the durations of action potentials in the presence of adenosine. Clamp pulse could reverse adenosine-induced but not cadmium chloride-induced decreases in twitch amplitude. Adenosine activated the inwardly rectifying K+ current (IK,Ado), but did not significantly decrease the L-type Ca2+ current (ICa,L). Adenosine reduced the effects of BAY K 8644 on APD90 and twitch amplitude but did not attenuate the BAY K-induced increase in ICa,L. The effects of adenosine on APD90 and twitch amplitude could be reversed after activation of IK,Ado was inhibited by intracellular application of cesium and tetraethylammonium chloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of interleukin 5-induced pulmonary eosinophilia on airway reactivity in the guinea pig

1996 ◽  
Vol 270 (3) ◽  
pp. L368-L375 ◽  
Author(s):  
C. M. Lilly ◽  
R. W. Chapman ◽  
S. J. Sehring ◽  
P. J. Mauser ◽  
R. W. Egan ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Histological Grade ◽  
Platelet Activating Factor ◽  
Inflammatory Cells ◽  
Dependent Manner ◽  
Interleukin 5 ◽  
Dose Dependent

Administration of interleukin 5 (IL-5) to guinea pigs by tracheal injection was associated with increased recovery of eosinophils and neutrophils from bronchoalveolar lavage (BAL) fluid. The number of eosinophils recovered from BAL fluid increased in a dose-dependent manner from 9 +/- 2 X 10(3)/ml to a plateau of 143 +/- 29 X 10(3)/ml after the administration of recombinant human IL-5 (rhIL-5). Tracheal administration of recombinant guinea pig IL-5 (gpIL-5) also increased eosinophil recovery but was less potent than rhIL-5. Histological analysis confirmed the presence of inflammatory cells in the lung; there were higher grades of inflammation in airway than in parenchymal tissue after gpIL-5 administration. In addition, the histological grade of airway inflammation was greater 24 and 72 h after gpIL-5 administration than it was 6 days after administration. Airway hyperresponsiveness is reported to occur in guinea pigs exposed to rhIL-5 by intraperitoneal cellular production. It is surprising that airway infiltration with eosinophils induced by the topical application of IL-5 was not associated with hyperresponsiveness to substance P, histamine, or platelet-activating factor in intact animals or to methacholine in tracheally perfused lungs. Furthermore, the microvascular leakage induced by substance P was not altered by rhIL-5 administration. These findings indicate that the presence of eosinophils alone is not sufficient for the expression of airway hyperresponsiveness. Our ability to separate eosinophil recruitment and retention in the tissues from airway hyperresponsiveness indicates that these two processes are distinct and that the presence of eosinophils in lung tissue, by itself, is not sufficient to alter airway contractile responses.

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