Ion channels and membrane potential in stimulus–secretion coupling in adrenal paraneurons

1984 ◽  
Vol 62 (5) ◽  
pp. 477-483 ◽  
Author(s):  
Daniel L. Kilpatrick
Keyword(s):  
Membrane Potential ◽  
Ion Channels ◽  
Adrenal Medulla ◽  
Nicotinic Receptor ◽  
Calcium Influx ◽  
Inhibitory Effect ◽  
Muscle Membrane ◽  
Bovine Adrenal Medulla ◽  
Voltage Dependent ◽  
Stimulus Secretion Coupling

Cultured bovine adrenal medulla cells have been shown to contain several different ion channels (Na+, Ca2+ acetylcholine receptor regulated) whose activation leads to the secretion of catecholamines. The pharmacology of these ion channels and their interactions during secretion have been examined. The mechanisms of agonist-induced calcium influx are of particular interest since this is an early obligatory event during secretion from the adrenal medulla. Data obtained on catecholamine release and 45Ca2+ uptake indicate that both voltage-dependent and voltage-independent calcium influx mechanisms operate in cultured bovine adrenal medulla cells. The significance of these results in understanding the mechanism of action of the physiological stimulus acetylcholine (Ach) will be discussed. The alkaloid channel neurotoxins D-600, batrachotoxin, veratridine, and aconitine were shown to exert a noncompetitive inhibitory effect on Ach-induced ion flux in adrenal medulla cells, presumably through an interaction with the nicotinic receptor regulated channel. Lipid-soluble neurotoxins may interact with multiple ion channels in nerve and muscle membrane.

scholarly journals Protein kinase C (PKC) and down-regulation of voltage-dependent Na channel in bovine adrenal medulla cells.

1994 ◽  
Vol 64 ◽  
pp. 305
Author(s):  
Toshihiko Yanagita ◽  
Ryuichi Yamamoto ◽  
Tomoaki Yuhi ◽  
Masanobu Urabe ◽  
Hiromi Niina ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adrenal Medulla ◽  
Na Channel ◽  
Down Regulation ◽  
Bovine Adrenal Medulla ◽  
Kinase C ◽  
Voltage Dependent

Efflux of 45Ca from bovine adrenal medulla cells inculture caused by nicotinic receptor stimulation

1984 ◽  
Vol 47 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Akihiko Wada ◽  
Futoshi Izumi ◽  
Noriko Yashima ◽  
Hideyuki Kobayashi ◽  
Yumiko Toyohira ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Nicotinic Receptor ◽  
Receptor Stimulation ◽  
Bovine Adrenal Medulla

Regulation of membrane potential and diameter by voltage-dependent K+ channels in rabbit myogenic cerebral arteries

1995 ◽  
Vol 269 (1) ◽  
pp. H348-H355 ◽  
Author(s):  
H. J. Knot ◽  
M. T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Transmural Pressure ◽  
Muscle Membrane ◽  
K Channels ◽  
Wide Range ◽  
Voltage Dependent

The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) cerebral arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these arteries depolarized and the arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized cerebral arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) cerebral arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small cerebral arteries to changes in intravascular pressure.

Ion channels in smooth muscle: regulators of intracellular calcium and contractility

2005 ◽  
Vol 83 (3) ◽  
pp. 215-242 ◽  
Author(s):  
Kevin S Thorneloe ◽  
Mark T Nelson
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Membrane Potential ◽  
Ion Channels ◽  
Feedback Mechanism ◽  
Negative Feedback Mechanism ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Active Channels ◽  
Trisphosphate Receptor

Smooth muscle (SM) is essential to all aspects of human physiology and, therefore, key to the maintenance of life. Ion channels expressed within SM cells regulate the membrane potential, intracellular Ca2+ concentration, and contractility of SM. Excitatory ion channels function to depolarize the membrane potential. These include nonselective cation channels that allow Na+ and Ca2+ to permeate into SM cells. The nonselective cation channel family includes tonically active channels (Icat), as well as channels activated by agonists, pressure-stretch, and intracellular Ca2+ store depletion. Cl--selective channels, activated by intracellular Ca2+ or stretch, also mediate SM depolarization. Plasma membrane depolarization in SM activates voltage-dependent Ca2+ channels that demonstrate a high Ca2+ selectivity and provide influx of contractile Ca2+. Ca2+ is also released from SM intracellular Ca2+ stores of the sarcoplasmic reticulum (SR) through ryanodine and inositol trisphosphate receptor Ca2+ channels. This is part of a negative feedback mechanism limiting contraction that occurs by the Ca2+-dependent activation of large-conductance K+ channels, which hyper polarize the plasma membrane. Unlike the well-defined contractile role of SR-released Ca2+ in skeletal and cardiac muscle, the literature suggests that in SM Ca2+ released from the SR functions to limit contractility. Depolarization-activated K+ chan nels, ATP-sensitive K+ channels, and inward rectifier K+ channels also hyperpolarize SM, favouring relaxation. The expression pattern, density, and biophysical properties of ion channels vary among SM types and are key determinants of electrical activity, contractility, and SM function.Key words: smooth muscle, ion channel, membrane potential, calcium, contraction.

Contracture and change in membrane potential produced by sodium removal in the dog trachea and bronchiole

1989 ◽  
Vol 67 (5) ◽  
pp. 2078-2086 ◽  
Author(s):  
Y. Ito ◽  
T. Inoue
Keyword(s):  
Membrane Potential ◽  
Mechanical Response ◽  
Muscle Tone ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Tetraacetic Acid ◽  
Mechanical Responses ◽  
Sodium Removal ◽  
Voltage Dependent ◽  
Smooth Muscle Membrane

Mechanical responses and changes in membrane potential induced by Na removal were investigated in dog tracheal and bronchiolar smooth muscles. In both muscles, reduction of the external Na concentration ([Na]o) to less than 70 mM produced a sustained contracture, dose dependently. The relative amplitude of the Na-free contracture was greater than that induced by excess [K]o in the trachealis. Readmission of 1-10 mM Na, after exposure to Na-free solution, relaxed the contracture evoked by Na removal, and the degree of relaxation was dependent on [Na] readmitted. In the absence of both Na and Ca, some tension remained, and readmission of Ca increased the muscle tone. Even after pretreatment with Ca-free ethylene glycol-bis (beta-aminoethylether)-N,N,N,N′-tetraacetic acid- (0.2 mM) containing solution for 30 min, removal of Na caused some mechanical response in both muscles. D 600 (10(-7) to 10(-4) M), a blocker of voltage-dependent Ca2+ influx, suppressed the response to Na removal, but 10(-4) M D 600 did not completely block the contracture. Na removal depolarized the smooth muscle membrane to a greater extent in the bronchiole than in the trachealis. It was concluded that an increase in Ca permeability across the membrane and inhibition of the Na-Ca exchange mechanism in the absence of Na are responsible for the generation of Na-free contracture in both muscles.

scholarly journals Lysophosphatidylchollne Inhibition of ion channels and catecholamine secretion in bovine adrenal medulla.

1991 ◽  
Vol 55 ◽  
pp. 170
Author(s):  
Futoshi Izumi ◽  
Yumiko Toyohira ◽  
Nobuyuki Yanagihara ◽  
Yasuhito Uezono ◽  
Yoshiro Koda ◽  
...  
Keyword(s):  
Ion Channels ◽  
Adrenal Medulla ◽  
Catecholamine Secretion ◽  
Bovine Adrenal Medulla
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