Voltage-dependent blockade in Na+-dependent action potentials after β1- and H2-receptor stimulation in mammalian ventricular myocardium

1988 ◽  
Vol 66 (10) ◽  
pp. 1291-1296 ◽  
Author(s):  
A. M. Gillis ◽  
M. Kohlhardt
Keyword(s):  
Action Potentials ◽  
Ventricular Myocardium ◽  
Inhibitory Effect ◽  
Receptor Blocker ◽  
Control Value ◽  
Relationship Analysis ◽  
Adrenoceptor Agonist ◽  
Voltage Dependent ◽  
Initial Control ◽  
Β Receptor

In isolated papillary muscles of guinea pigs, the influence of isoproterenol, histamine, theophylline, and phenylephrine on the maximal rate of rise [Formula: see text] of Na+-dependent action potentials and on isometric contractile force was studied under rested state conditions. Isoproterenol (1 × 10−7 mol/L), histamine (2 × 10−5 mol/L), and theophylline (2 × 10−3 mol/L) shifted the voltage dependence of [Formula: see text] into the hyperpolarizing direction and, consequently, led to a voltage-dependent [Formula: see text] blockade. The α-adrenoceptor agonist phenylephrine, on the other hand, proved to be ineffective in depressing [Formula: see text]. The β-receptor blocker pindolol (4 × 10−6 mol/L) or the H2-receptor blocker cimetidine (4 × 10−5 mol/L) abolished the inhibitory effects of isoproterenol and histamine, respectively, and caused [Formula: see text] to return to the initial control value. A concentration–response relationship analysis at −65 mV revealed that isoproterenol exerted only a weak inhibitory effect on [Formula: see text] compared with its positive inotropic action. The IC50 value of the former effect amounted to approximately 5 × 10−6 mol/L, but the EC50 value of the latter effect was 4 × 10−8 mol/L. It is, therefore, concluded that, in physiologically relevant concentrations, β-adrenergic agonists are unlikely to significantly modulate Na+-dependent excitability even in partially depolarized myocardium.

Effects of bromocriptine on prolactin release, electrical membrane properties and transmembrane Ca2+ fluxes in cultured rat pituitary adenoma cells

1986 ◽  
Vol 111 (2) ◽  
pp. 185-192 ◽  
Author(s):  
P. W. Johansen ◽  
O. Sand ◽  
J. G. Iversen ◽  
E. Haug ◽  
K. M. Gautvik
Keyword(s):  
Pituitary Adenoma ◽  
Action Potentials ◽  
Inhibitory Effect ◽  
Membrane Properties ◽  
Free Solution ◽  
Prolactin Release ◽  
Clonal Strain ◽  
Rat Pituitary ◽  
Basal Release ◽  
Voltage Dependent

Abstract. The effects of the dopamine (DA) agonist bromocriptine on prolactin (Prl) release, electrical membrane properties and transmembrane Ca2 + fluxes have been studied in a clonal strain of rat pituitary adenoma cells (GH3). These cells generate Ca2+ dependent action potentials, and produce and secrete spontaneously both Prl and growth hormone. Prl release stimulated by thyroliberin (TRH) and elevated extracellular K+ concentration was completely blocked by bromocriptine, whereas the basal release was only moderately affected. The TRH and K+ evoked Prl release were half maximally inhibited by bromocriptine at 5–10 and 10–50 μm, respectively. The normal biphasic membrane response to TRH and the depolarizing effect of elevated K+ concentration were not altered by bromocriptine, whereas the Ca2+-spikes in Na+-free solution were suppressed by the drug. We therefore suggest that bromocriptine blocks the voltage sensitive Ca2+-channels of GH3 cells. In agreement with this notion, bromocriptine also suppressed the basal and TRH induced 45Ca2+ efflux from preloaded cells. We conclude that the inhibitory effect of bromocriptine on the voltage dependent Ca2+-channels is an important mechanism responsible for suppression of Prl release.

Nitric oxide induces [Ca2+]i oscillations in pituitary GH3 cells: involvement of IDR and ERG K+ currents

2006 ◽  
Vol 290 (1) ◽  
pp. C233-C243 ◽  
Author(s):  
Agnese Secondo ◽  
Anna Pannaccione ◽  
Mauro Cataldi ◽  
Rossana Sirabella ◽  
Luigi Formisano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect ◽  
Receptor Blocker ◽  
Gh3 Cells ◽  
No Donors ◽  
Quiescent Cells ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Trisphosphate Receptor

The role of nitric oxide (NO) in the occurrence of intracellular Ca2+ concentration ([Ca2+]i) oscillations in pituitary GH3 cells was evaluated by studying the effect of increasing or decreasing endogenous NO synthesis with l-arginine and nitro-l-arginine methyl ester (l-NAME), respectively. When NO synthesis was blocked with l-NAME (1 mM) [Ca2+]i, oscillations disappeared in 68% of spontaneously active cells, whereas 41% of the quiescent cells showed [Ca2+]i oscillations in response to the NO synthase (NOS) substrate l-arginine (10 mM). This effect was reproduced by the NO donors NOC-18 and S-nitroso- N-acetylpenicillamine (SNAP). NOC-18 was ineffective in the presence of the L-type voltage-dependent Ca2+ channels (VDCC) blocker nimodipine (1 μM) or in Ca2+-free medium. Conversely, its effect was preserved when Ca2+ release from intracellular Ca2+ stores was inhibited either with the ryanodine-receptor blocker ryanodine (500 μM) or with the inositol 1,4,5-trisphosphate receptor blocker xestospongin C (3 μM). These results suggest that NO induces the appearance of [Ca2+]i oscillations by determining Ca2+ influx. Patch-clamp experiments excluded that NO acted directly on VDCC but suggested that NO determined membrane depolarization because of the inhibition of voltage-gated K+ channels. NOC-18 and SNAP caused a decrease in the amplitude of slow-inactivating ( IDR) and ether-à-go-go-related gene ( ERG) hyperpolarization-evoked, deactivating K+ currents. Similar results were obtained when GH3 cells were treated with l-arginine. The present study suggests that in GH3 cells, endogenous NO plays a permissive role for the occurrence of spontaneous [Ca2+]i oscillations through an inhibitory effect on IDR and on IERG.

Transducer properties of atrial receptors in the dog after 60 min of increased atrial pressure

1981 ◽  
Vol 59 (8) ◽  
pp. 837-842 ◽  
Author(s):  
C. T. Kappagoda ◽  
M. Padsha
Keyword(s):  
Action Potentials ◽  
Control Period ◽  
Atrial Pressure ◽  
Response Curves ◽  
Experimental Conditions ◽  
Stimulus Response ◽  
Control Value ◽  
Significant Difference ◽  
Initial Control ◽  
Atrial Receptors

This investigation was undertaken to examine the effect of a period of increased atrial pressure lasting 60 min on the ability of atrial receptors to transduce changes in atrial pressure. The experiments were performed on dogs anesthetized with pentobarbitone. Action potentials were recorded from branches of the cervical vagi and the atrial pressure was increased by distending a balloon in the lumen of the left atrium. Twelve receptors were examined in 14 dogs. For each receptor, stimulus–response curves relating the action potentials generated (number per cardiac cycle) to the mean left atrial pressure (centimetres of H2O) were obtained under three experimental conditions: (a) during an initial control period, (b) after 60 min of increased atrial pressure (i.e. 10–12 cm H2O), and (c) 60 min after restoration of the atrial pressure to its control value. It was found that in all 12 units the ability of the receptors to transduce changes in atrial pressure was impaired after 60 min of increased atrial pressure, i.e., the number of action potentials generated by a receptor for the same atrial pressure was smaller than that in the control period. This effect was partially restored in the 12 units 60 min after restoration of the atrial pressures to their respective control values.In four units the stimulus–response curves were repeated 60 min after obtaining the initial control response. It was found that there was no significant difference in each pair of curves. It is concluded that relatively short periods of increased atrial pressure impair transducer properties of the atrial receptors.

Inhibitory effect of adrenaline on oxytocin release in the ewe during the milk-ejection reflex

1979 ◽  
Vol 46 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Tadeusz Barowicz
Keyword(s):  
Blood Plasma ◽  
Milk Yield ◽  
Myoepithelial Cell ◽  
Inhibitory Effect ◽  
Receptor Blocker ◽  
Milk Ejection ◽  
Cell Level ◽  
Oxytocin Release ◽  
Milk Ejection Reflex ◽  
Β Receptor

SUMMARYMilk-ejection activity was determined in the blood plasma of ewes during normal milking and during milking when adrenaline was injected intravenously before or after udder stimulation. It was found that administration of adrenaline either before or after udder washing, decreased the oxytocin concentration and milk yield but increased the yield by hand-stripping. Adrenaline also retards the average time for peak oxytocin concentration. These results and the use of a β-receptor blocker to inhibit the effect of adrenaline at the myoepithelial cell level indicate that in ewes adrenaline can prevent the release of oxytocin from neurohypophysis.

β-Receptor Blocker Withdrawal. A Preoperative Problem in General Surgery?

1982 ◽  
Vol 26 ◽  
pp. 32-37 ◽  
Author(s):  
J. Pontén ◽  
B. Biber ◽  
T. Bjurö ◽  
B-Å. Henriksson ◽  
Å. Hjalmarson
Keyword(s):  
General Surgery ◽  
Receptor Blocker ◽  
Β Receptor

Electrical Properties and Anion Permeability of Doubly Rectifying Junctions in the Leech Central Nervous System

1988 ◽  
Vol 137 (1) ◽  
pp. 1-11
Author(s):  
Susan E. Acklin
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
T Cell ◽  
Action Potentials ◽  
Sodium Pump ◽  
Current Flow ◽  
Cell Movement ◽  
Voltage Dependent ◽  
Electrical Connections

A study has been made of the electrical connections between touch sensory (T) neurones in the leech central nervous system (CNS) which display remarkable double rectification: depolarization spreads in both directions although hyperpolarization spreads poorly. Tests were made to determine whether this double rectification was a property of the junctions themselves or whether it resulted from changes in the length constants of processes intervening between the cell body and the junctions. Following trains of action potentials, T cells and their fine processes within the neuropile became hyperpolarized through the activity of an electrogenie sodium pump. When any T cell was hyperpolarized by 25 mV by repetitive stimulation, hyperpolarization failed to spread to the T cells to which it was electrically coupled. Further evidence for double rectification of junctions linking T cells was provided by experiments in which Cl− was injected electrophoretically. Cl− injection into one T cell caused inhibitory potentials recorded in it to become reversed. After a delay, Cl− spread to reverse IPSPs in the coupled T cell. Movement of Cl−, like current flow, was dependent on membrane potential. When the T cell into which Cl− was injected was kept hyperpolarized, Cl− failed to move into the adjacent T cell. Upon release of the hyperpolarization in the injected T cell, Cl− moved and reversed IPSPs in the coupled T cell. Together these results indicate that the gating properties of channels linking T cells are voltage-dependent, such that depolarization of either cell allows channels to open whereas hyperpolarization causes them to close.

scholarly journals Modulation of High-Voltage Activated Ca2+ Channels in the Rat Periaqueductal Gray Neurons by μ-Type Opioid Agonist

1997 ◽  
Vol 77 (3) ◽  
pp. 1418-1424 ◽  
Author(s):  
Chang-Ju Kim ◽  
Jeong-Seop Rhee ◽  
Norio Akaike
Keyword(s):  
G Proteins ◽  
Opioid Receptor ◽  
High Voltage ◽  
Inhibitory Effect ◽  
Periaqueductal Gray ◽  
Dependent Manner ◽  
Opioid Agonist ◽  
Voltage Clamp Condition ◽  
Voltage Dependent ◽  
Clamp Condition

Kim, Chang-Ju, Jeong-Seop Rhee, and Norio Akaike. Modulation of high-voltage activated Ca2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol. 77: 1418–1424, 1997. The effect of μ-type opioid receptor agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 118 PAG neurons tested, the HVA Ca2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of ω-conotoxin-GVIA occluded the inhibitory effect of DAMGO ∼70%. So, HVA Ca2+ channels inhibited by DAMGO were mainly the N-type Ca2+ channels. The inhibitory effect of DAMGO on HVA Ca2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8–10 h, suggesting that DAMGO modulation on N-type Ca2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that μ-type opioid receptor modulates N-type HVA Ca2+ channels via PTX-sensitive G proteins in PAG neurons of rats.

Simulator for neural networks and action potentials: description and application

1994 ◽  
Vol 71 (1) ◽  
pp. 294-308 ◽  
Author(s):  
I. Ziv ◽  
D. A. Baxter ◽  
J. H. Byrne
Keyword(s):  
Neural Networks ◽  
Central Pattern Generator ◽  
Action Potentials ◽  
Modular Design ◽  
Second Messenger ◽  
Pattern Generator ◽  
Slow Inward Current ◽  
Synaptic Connections ◽  
Different Types ◽  
Voltage Dependent

1. We describe a simulator for neural networks and action potentials (SNNAP) that can simulate up to 30 neurons, each with up to 30 voltage-dependent conductances, 30 electrical synapses, and 30 multicomponent chemical synapses. Voltage-dependent conductances are described by Hodgkin-Huxley type equations, and the contributions of time-dependent synaptic conductances are described by second-order differential equations. The program also incorporates equations for simulating different types of neural modulation and synaptic plasticity. 2. Parameters, initial conditions, and output options for SNNAP are passed to the program through a number of modular ASCII files. These modules can be modified by commonly available text editors that use a conventional (i.e., character based) interface or by an editor incorporated into SNNAP that uses a graphical interface. The modular design facilitates the incorporation of existing modules into new simulations. Thus libraries can be developed of files describing distinctive cell types and files describing distinctive neural networks. 3. Several different types of neurons with distinct biophysical properties and firing properties were simulated by incorporating different combinations of voltage-dependent Na+, Ca2+, and K+ channels as well as Ca(2+)-activated and Ca(2+)-inactivated channels. Simulated cells included those that respond to depolarization with tonic firing, adaptive firing, or plateau potentials as well as endogenous pacemaker and bursting cells. 4. Several types of simple neural networks were simulated that included feed-forward excitatory and inhibitory chemical synaptic connections, a network of electrically coupled cells, and a network with feedback chemical synaptic connections that simulated rhythmic neural activity. In addition, with the use of the equations describing electrical coupling, current flow in a branched neuron with 18 compartments was simulated. 5. Enhancement of excitability and enhancement of transmitter release, produced by modulatory transmitters, were simulated by second-messenger-induced modulation of K+ currents. A depletion model for synaptic depression was also simulated. 6. We also attempted to simulate the features of a more complicated central pattern generator, inspired by the properties of neurons in the buccal ganglia of Aplysia. Dynamic changes in the activity of this central pattern generator were produced by a second-messenger-induced modulation of a slow inward current in one of the neurons.

U46619, a thromboxane A2 agonist, inhibits KCa channel activity from pig coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. C708-C713 ◽  
Author(s):  
F. S. Scornik ◽  
L. Toro
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Lipid Bilayers ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Channel Activity ◽  
Open Probability ◽  
Control Value ◽  
Kca Channels ◽  
Internal Side

Thromboxane A2 (TxA2) is a potent vasoconstrictor derived from the metabolism of arachidonic acid. Because potassium channels are involved in the contraction of vascular smooth muscle, their blockade could contribute to the TxA2-induced contraction. To test this possibility, we studied the effect of the TxA2 stable analogue U46619 on calcium-activated potassium (KCa) channels from coronary artery reconstituted into lipid bilayers. Addition of U46619 (50-150 nM) to the external but not to the internal side of the channel decreased the channel open probability (Po) between 15 and 80% of the control value. The inhibitory effect of U46619 affected both the open and closed states of the channel and could be reversed by internal calcium. Thromboxane B2, the inactive hydrolysis derivative of TxA2, did not affect channel activity. SQ 29548, a TxA2 receptor antagonist, was able to prevent the inhibition by U46619. Furthermore, SQ 29548 added after U46619 could restore channel activity to near control values. These results suggest that TxA2 could be a regulatory factor of KCa channels from coronary smooth muscle and that this regulation could be related to its action as a vasoconstrictor.

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