scholarly journals Electrical and Mechanical Changes during Anoxic Contractions of the Isolated Canine Basilar Artery

1993 ◽  
Vol 13 (3) ◽  
pp. 498-502 ◽  
Author(s):  
Tetsuhiko Nagao ◽  
Paul M. Vanhoutte
Keyword(s):  
Membrane Potential ◽  
Basilar Artery ◽  
Membrane Depolarization ◽  
Isometric Tension ◽  
Free Solution ◽  
High K ◽  
Voltage Dependent ◽  
Canine Basilar Artery

Isometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca2+-channel inhibitor, diltiazem, and were abolished in Ca2+-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage-dependent Ca2 + influx in the generation of anoxic contractions in the canine basilar artery. However, membrane depolarization does not fully account for these anoxic contractions.

scholarly journals Low-voltage activated (LVA) inward current in murine antral smooth muscle cells is an artifact

2021 ◽  
Author(s):  
Ji Yeon Lee ◽  
Haifeng Zheng ◽  
Kenton M. Sanders ◽  
Sang Don Koh
Keyword(s):  
Low Voltage ◽  
External Solution ◽  
Physiological Salt Solution ◽  
Channel Blockers ◽  
Free Solution ◽  
Inward Current ◽  
High K ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Rich Solution

We characterized the two types of voltage-dependent inward currents in murine antral SMC. The HVA and LVA inward currents were identified when cells were bathed in Ca2+-containing physiological salt solution. We examined whether the LVA inward current was due to: 1) T-type Ca2+ channels, 2) Ca2+-activated Cl- channels, 3) non-selective cation channels (NSCC) or 4) voltage-dependent K+ channels with internal Cs+-rich solution. Replacement of external Ca2+ (2 mM) with equimolar Ba2+ increased the amplitude of the HVA current but blocked the LVA current. Nicardipine blocked the HVA current, and in the presence of nicardipine, T-type Ca2+ blockers failed to block LVA. The Cl- channel antagonist had little effect on LVA. Cation-free external solution completely abolished both HVA and LVA. Addition of Ca2+ in cation-free solution restored only HVA currents. Addition of K+ (5 mM) to cation-free solution induced LVA current that reversed at -20 mV. These data suggest that LVA is not due to T-type Ca2+ channels, Ca2+-activated Cl- channels or NSCC. Antral SMC express A-type K+ currents (KA) and delayed rectifying K+ currents (KV) with dialysis of high K+ (140 mM) solution. When cells were exposed to high K+ external solution with dialysis of Cs+-rich solution in the presence of nicardipine, LVA was evoked and reversed at positive potentials. These HK-induced inward currents were blocked by K+ channel blockers, 4-aminopyridine and TEA. In conclusion, LVA inward currents can be generated by K+ influx via KA and KV channels in murine antral SMC when cells were dialyzed with Cs+-rich solution.

scholarly journals Mechanism of the Enhanced Vasoconstrictor Responses to Endothelin-1 in Canine Cerebral Arteries

1991 ◽  
Vol 11 (3) ◽  
pp. 371-379 ◽  
Author(s):  
Chiharu Tanoi ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Kenichiro Sugita ◽  
Kaoru Masuzawa ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Resting State ◽  
Mesenteric Artery ◽  
Cerebral Arteries ◽  
Mesenteric Arteries ◽  
Free Solution ◽  
Contractile Responses ◽  
Endothelin 1 ◽  
Voltage Dependent ◽  
Small Contraction

Vasoconstrictor effects of endothelin-1 (ET) were investigated in endothelium-denuded strips of cerebral (basilar and posterior cerebral) and mesenteric arteries of the dog. ET produced a concentration-dependent contraction in these arteries. Contractile responses to lower concentrations (below 3 × 10−10 M) of ET were significantly greater in the cerebral arteries than in the mesenteric artery. Inhibition by nifedipine of the contractile responses to ET was greater in the basilar artery than in the mesenteric artery. After the inhibition by 10−7 M nifedipine, the remaining responses to ET were similar in the two arteries. Cerebral arteries, but not the mesenteric artery, relaxed significantly from the resting level when placed in a Ca2+ -free solution containing 0.1 m M EGTA (0-Ca solution). Readdition of Ca2+ to the cerebral arteries placed in the 0-Ca solution caused a biphasic contraction that was sensitive to nifedipine. When 10−9 M ET was introduced before the Ca2+-induced contraction, this peptide produced only a very small contraction, but enhanced the Ca2+-induced contraction. The extent of the enhancement induced by ET was much greater in the cerebral arteries than in the mesenteric artery. These results indicate that the enhanced responses to ET in the cerebral arteries were dependent to a large extent on Ca2+ influx through voltage-dependent Ca2+ channels (VDCs). It is likely that the VDCs in these arteries are more activated in the resting state than those in the mesenteric artery.

Inhibition of Na+/H+exchange stimulates CCK secretion in STC-1 cells

1998 ◽  
Vol 275 (4) ◽  
pp. G689-G695
Author(s):  
Veronica Prpic ◽  
J. Gregory Fitz ◽  
Yu Wang ◽  
John R. Raymond ◽  
Maria N. Garnovskaya ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cell Metabolism ◽  
Hormone Secretion ◽  
Membrane Depolarization ◽  
Ph Sensitive ◽  
Extracellular Medium ◽  
Voltage Dependent ◽  
Effects Of Ph ◽  
Intracellular Ca ◽  
Cck Release

It has been demonstrated that K+ channel regulation of membrane potential is critical for control of CCK secretion. Because certain K+ channels are pH sensitive, it was postulated that pH affects K+channel activity in the CCK-secreting cell line STC-1 and may participate in regulating CCK secretion. The present study examines the role of electroneutral Na+/H+exchange on extracellular acidification and hormone secretion. Treatment of STC-1 cells with the amiloride analog ethylisopropyl amiloride (EIPA) to inhibit Na+/H+exchange inhibited Na+-dependent H+ efflux and increased basal CCK secretion. Substituting choline for NaCl in the extracellular medium elevated basal intracellular Ca2+concentration and stimulated CCK release. Stimulatory effects on hormone secretion were blocked by the L-type Ca2+ channel blocker diltiazem, indicating that secretion was dependent on the influx of extracellular Ca2+. To determine whether the effects of EIPA and Na+ depletion were due to membrane depolarization, we tested graded KCl concentrations. The ability of EIPA to increase CCK secretion was inhibited by depolarization induced by 10–50 mM KCl in the bath. Maneuvers to lower intracellular pH (pHi), including reducing extracellular pH (pHo) to 7.0 or treatment with sodium butyrate, significantly increased CCK secretion. To examine whether pH directly affects membrane K+ permeability, we measured outward currents carried by K+, using whole cell patch techniques. K+ current was significantly inhibited by lowering pHo to 7.0. These effects appear to be mediated through changes in pHi, because intracellular dialysis with acidic solutions nearly eliminated current activity. These results suggest that Na+/H+exchange and membrane potential may be functionally linked, where inhibition of Na+/H+exchange lowers pHi and depolarizes the membrane, perhaps through inhibition of pH-sensitive K+ channels. In turn, K+ channel closure and membrane depolarization open voltage-dependent Ca2+ channels, leading to an increase in cytosolic Ca2+ and CCK release. The effects of pHi on K+ channels may serve as a potent stimulus for hormone secretion, linking cell metabolism and secretory functions.

Distribution and functional properties of glutamate receptors in the leech central nervous system

1996 ◽  
Vol 75 (6) ◽  
pp. 2312-2321 ◽  
Author(s):  
P. W. Dierkes ◽  
P. Hochstrate ◽  
W. R. Schlue
Keyword(s):  
Glutamate Receptors ◽  
Glial Cells ◽  
Membrane Depolarization ◽  
Free Solution ◽  
Fluorescent Indicators ◽  
Intracellular Na Activity ◽  
Bath Application ◽  
Voltage Dependent ◽  
Ion Sensitive Microelectrodes ◽  
Ca2 Channels

1. The effect of kainate and other glutamatergic agonists on the membrane potential (Em), the intracellular Na+ activity (aNai), and the intracellular free Ca2+ concentration ([Ca2+]i) of identified leech neurons and neuropile glial cells was measured with conventional and ion-sensitive microelectrodes, as well as with the use of the iontophoretically injected fluorescent indicators sodium-binding benzofuran isophthalate and Fura-2. 2. In Retzius neurons, AE, L, 8, and 101 motoneurons, and in the unclassified 50 neurons (Leydig cells) and AP neurons, as well as in neuropile glial cells, bath application of 100 microM kainate evoked a marked membrane depolarization and an increase in aNai and [Ca2+]i. The kainate-induced aNai increase persisted in solutions with high Mg2+ concentration in which synaptic transmission is blocked. 3. A membrane depolarization as well as an increase in aNai and [Ca2+]i was also evoked by L-glutamate, quisqualate, and L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). The agonist-induced [Ca2+]i increase was inhibited by 6,7-dinitroquinoxaline-2,3-dione (DNQX). 4. In Ca(2+)-free solution, the kainate-induced [Ca2+]i increase was abolished in the neurons and in neuropile glial cells, whereas membrane depolarization and aNai increase were unchanged. In Na(+)-free solution, kainate had no effect on Em, aNai, or [Ca2+]i in the neurons. 5. In the mechanosensory T, P, and N neurons, kainate induced considerably smaller membrane depolarizations than in the other neurons or in neuropile glial cells, and it had no significant effect on aNai or [Ca2+]i. 6. It is concluded that in leech segmental ganglia the majority of the neurons and the neuropile glial cells, but probably not the mechanosensory neurons, possess glutamate receptors of the AMPA-kainate type. In the neurons, the [Ca2+]i increase caused by glutamatergic agonists is due to Ca2+ influx through voltage-dependent Ca2+ channels that are activated by the agonist-induced membrane depolarization.

Physiology of obliquely striated muscle fibres within Grillotia erinaceus metacestodes (Cestoda: Trypanorhyncha)

Parasitology ◽  
1992 ◽  
Vol 104 (2) ◽  
pp. 337-346 ◽  
Author(s):  
S. M. Ward ◽  
J. M. Allen ◽  
G. McKerr
Keyword(s):  
Striated Muscle ◽  
Membrane Depolarization ◽  
Isometric Tension ◽  
Equilibrium Potential ◽  
Muscle Fibres ◽  
High K ◽  
Motor End Plates ◽  
Intracellular Microelectrodes ◽  
High Concentrations ◽  
Grillotia Erinaceus

SUMMARYThe tentacular bulb of Grillotia erinaceus metacestodes consists of obliquely striated muscle fibres with obvious motor end-plates. In this study isometric tension recordings and intracellular microelectrodes have been used to record mechanical and electrical activity from single isolated bulbs. Bulbs were mechanically quiescent and displayed resting membrane polentials (RMP) in the region of −49 to −64 mV with a mean RMP of −56 mV (n = 60). The membrane potential varied with [K+]o in a manner consistent with the RMP being determined largely by the K+ equilibrium potential. High K+ solution (> 15 mM) caused membrane depolarization and contraction of the preparation with the contraction showing both phasic and tonic components. L-glutamate caused membrane depolarization, contraction of quiescent preparations and increased the amplitude of electrically evoked responses. In contrast, 5-HT, dopamine, histamine, adrenaline, GABA, noradrenaline and D-glutamate, at concentrations up to and including 10−3 M, were without apparent affect, although acetylcholine, at relatively high concentrations (≥ 10−4 M) slightly reduced the amplitude of field-evoked contractions.

Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery

1993 ◽  
Vol 264 (2) ◽  
pp. H413-H418 ◽  
Author(s):  
F. Cosentino ◽  
J. C. Sill ◽  
Z. S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Nitric Oxide Donor ◽  
Basal Tone ◽  
Basilar Arteries ◽  
Canine Basilar Artery ◽  
Subsequent Activation ◽  
Oxide Synthase

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.

scholarly journals Nicotine Exposure, Mimicked Smoking, Directly and Indirectly Enhanced Protein Kinase C Activity in Isolated Canine Basilar Artery, Resulting in Enhancement of Arterial Contraction

2005 ◽  
Vol 25 (3) ◽  
pp. 292-301 ◽  
Author(s):  
Masayo Koide ◽  
Shigeru Nishizawa ◽  
Seiji Yamamoto ◽  
Mitsuo Yamaguchi ◽  
Hiroki Namba ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Basilar Artery ◽  
Vascular Endothelial Cells ◽  
Cerebrovascular Disorders ◽  
Significant Risk ◽  
Isometric Tension ◽  
Kinase C ◽  
Canine Basilar Artery ◽  
Arterial Tone

Cigarette smoking is a significant risk factor in the incidence of cerebrovascular disorders. Among the many compounds in cigarette smoke, nicotine is considered to most significantly affect cerebral arterial tone. The purpose of this study is to investigate precise pharmacological effects of nicotine on the regulation of cerebral arterial tone. To mimic smoking, a low concentration of nicotine (10−6 mol/L), which is equivalent to the serum level of habitual smokers, was treated for 1 hour in an isometric tension study and for 24 hours in a study using cultured vascular endothelial cells (VECs). Using the canine basilar artery, the effect of nicotine on uridine 5′-triphosphate (UTP)-induced vasoconstriction was examined in the isometric tension study. Protein kinase C (PKC) activity in the canine basilar artery was measured by enzyme immunoassay. Endothelial function was assessed by endothelium-dependent vasodilatation and endogenous nitric oxide (NO) synthesis in VECs using a fluorescent indicator, diaminofluorescein-FM diacetate (DAF-FM/DA). Nicotine significantly enhanced UTP-induced contraction and PKC activity in the artery, and attenuated endothelium-dependent vasodilatation and NO synthesis in VECs. Because PKC activity was increased by de-endothelialization itself, endothelial dysfunction by nicotine enhances PKC activity. Because PKC was further activated by nicotine even in the de-endothelialized artery, nicotine directly affects PKC activities in smooth muscle. These results indicate that nicotine potentiates contractile response through direct and indirect PKC activation in the canine basilar artery.

Role of Cl− current in endothelin-1-induced contraction in rabbit basilar artery

2001 ◽  
Vol 281 (5) ◽  
pp. H2159-H2167 ◽  
Author(s):  
Yun Dai ◽  
John H. Zhang
Keyword(s):  
Basilar Artery ◽  
Methanesulfonic Acid ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Free Solution ◽  
Bicarbonate Buffer ◽  
Endothelin 1 ◽  
New Zealand White Rabbits ◽  
Basilar Arteries

Cl− efflux induces depolarization and contraction of smooth muscle cells. This study was undertaken to explore the role of Cl− channels in endothelin-1 (ET-1)-induced contraction in rabbit basilar artery. Male New Zealand White rabbits ( n = 26), weighing 1.8–2.5 kg, were euthanized by an overdose of pentobarbital. The basilar arteries were removed for isometric tension recording. ET-1 produced a concentration-dependent contraction of the rabbit basilar artery in the normal Cl− Krebs-Henseleit bicarbonate buffer (123 mM Cl−). The ET-1-induced contraction was reduced by the following manipulations: 1) inhibition of Na+-K+-2Cl− cotransporter with bumetanide (3 × 10−5 and 10−4 M), 2) bicarbonate-free solution to disable Cl−/HCO[Formula: see text] exchanger, and 3) preincubation of rings with the Cl− channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino)benzoic acid, and indanyloxyacetic acid 94. The ET-1-induced contraction was enhanced by substitution of extracellular Cl− (10 mM) with methanesulfonic acid (113 mM). Cl− channels are involved in ET-1-induced contraction in the rabbit basilar artery.

Alteration in voltage-dependent calcium channels in dog basilar artery after subarachnoid hemorrhage

2010 ◽  
Vol 113 (4) ◽  
pp. 870-880 ◽  
Author(s):  
Elena Nikitina ◽  
Ayako Kawashima ◽  
Masataka Takahashi ◽  
Zhen-Du Zhang ◽  
Xueyuan Shang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Low Voltage ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Dose Effect ◽  
Voltage Dependent ◽  
Channel Currents ◽  
Number Of Cells

Object The L-type Ca++ channel antagonists like nimodipine have limited efficacy against vasospasm after subarachnoid hemorrhage (SAH). The authors tested the hypothesis that this is because SAH alters these channels, rendering them less responsible for contraction. Methods Basilar artery smooth muscle cells were isolated 4, 7, and 21 days after SAH in dogs, and Ca++ channel currents were recorded in 10-mmol/L barium. Proteins for α1 subunits of L-type Ca++ channels were measured by immunoblotting and isometric tension recordings done on rings of the basilar artery. Results High voltage–activated (HVA) Ca++ channel currents were significantly decreased and low voltage–activated (LVA) currents increased during vasospasm 4, 7, and 21 days after SAH (p < 0.05). Vasospasm was associated with a significant decrease in the number of cells with negligible LVA current while the number of cells in which the LVA current formed greater than 50% of the maximal current increased (p < 0.01). Window currents through LVA and HVA channels were significantly reduced. All changes correlated with the severity of vasospasm. There was an increase in protein for Cav3.1 and Cav3.3 α1 subunits that comprise T-type Ca++ channels, a decrease in L-type (Cav1.2 and Cav1.3) and an increase in R-type (Cav2.3) Ca++ channel α1 subunits. Functionally, however, isometric tension studies showed vasospastic arteries still relaxed with nimodipine. Conclusions Voltage-dependent Ca++ channels are altered in cerebral arteries after SAH. While decreased L-type channels may account for the lack of efficacy of nimodipine clinically, there may be other reasons such as inadequate dose, effect of nimodipine on other cellular targets, and mechanisms of vasospasm other than smooth muscle contraction mediated by activation of L-type Ca++ channels.

scholarly journals Partition of the organochlorine insecticide lindane into the human sperm surface induces membrane depolarization and Ca2+ influx

1997 ◽  
Vol 321 (3) ◽  
pp. 691-698 ◽  
Author(s):  
Leopoldo SILVESTRONI ◽  
Roberto FIORINI ◽  
Simonetta PALLESCHI
Keyword(s):  
Plasma Membrane ◽  
Human Sperm ◽  
Membrane Depolarization ◽  
Organochlorine Insecticide ◽  
Dipole Potential ◽  
Membrane Dipole Potential ◽  
High K ◽  
Voltage Dependent ◽  
Sperm Plasma Membrane ◽  
Influx Pathways

The effects of the insecticide lindane (the γ-isomer of 1,2,3,4,5,6-hexachlorocyclohexane) on membrane potential, cytosolic free Ca2+ concentration ([Ca2+]i) and surface biophysical properties were studied in human spermatozoa. The insecticide induces rapid, transient and reproducible membrane depolarization and opening of voltage-dependent Ca2+ channels leading to an increase in [Ca2+]i. In contrast with the effect in somatic cells, lindane did not affect γ-aminobutyric acid receptor-linked Cl- currents. Ca2+ and K+ currents were found to drive lindane-induced membrane depolarization and repolarization respectively, whereas Na+ and Cl- fluxes appear not to have a role in the phenomenon. The insecticide was still able to produce membrane depolarization both in the combined absence of extracellular Ca2+ and Na+ and in high-K+ buffer, suggesting that lindane alters the membrane dipole potential. In agreement with this, Laurodan and Prodan fluorescence spectroscopy revealed that lindane partition into the sperm plasma membrane lowers water molecular dynamics in the uppermost region of the membrane external leaflet, probably as the result of reordering of water dipoles. We propose that the first effect of lindane partitioning into the sperm plasma membrane is a change in the membrane dipole potential, which results in the activation of membrane-located Ca2+-influx pathways.

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