Isoprenaline-induced Relaxation of Smooth Muscle not due to Electrogenic Sodium Pumping

1972 ◽  
Vol 50 (4) ◽  
pp. 378-380 ◽  
Author(s):  
Deepak Bose ◽  
Ian R. Innes
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Sodium Pump ◽  
Free Medium ◽  
Electrogenic Sodium Pump ◽  
Sodium Pumping ◽  
Stimulation Of

Ouabain or replacement of NaCl by LiCl abolishes the relaxation due to addition of KCl to sodium-rich cat carotid artery strips kept in a K+-free medium. Neither treatment antagonizes the relaxation due to β-adrenoceptor stimulation by l-isoprenaline. Unlike KCl-induced relaxation, the relaxation induced by l-isoprenaline is not due to stimulation of an electrogenic sodium pump.

Endothelial Stimulation of Sodium Pump in Cultured Vascular Smooth Muscle

Hypertension ◽  
1995 ◽  
Vol 26 (1) ◽  
pp. 177-185 ◽  
Author(s):  
Juliana Redondo ◽  
Concepción Peiró ◽  
Leocadio Rodríguez-Mañas ◽  
Mercedes Salaices ◽  
Jesús Marín ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Sodium Pump ◽  
Stimulation Of

Monovalent Ion Specificity of the Electrogenic Sodium Pump in Vascular Smooth Muscle

1981 ◽  
Vol 166 (3) ◽  
pp. 457-461 ◽  
Author(s):  
R. C. Webb ◽  
W. E. Lockette ◽  
P. M. Vanhoutte ◽  
D. F. Bohr
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Sodium Pump ◽  
Ion Specificity ◽  
Electrogenic Sodium Pump ◽  
Monovalent Ion

Potassium and the recovery of splenic capsular smooth muscle after cold storage

1976 ◽  
Vol 54 (3) ◽  
pp. 322-326
Author(s):  
D. Bose ◽  
I. R. Innes
Keyword(s):  
Smooth Muscle ◽  
Ambient Temperature ◽  
Cold Storage ◽  
Sodium Pump ◽  
Intracellular Sodium ◽  
Free Medium ◽  
Bathing Medium ◽  
Cat Spleen ◽  
Sodium And Potassium ◽  
Low Ambient Temperature

Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

Microtubule disruption stimulates system A transport in cultured vascular smooth muscle cells

1995 ◽  
Vol 268 (6) ◽  
pp. C1512-C1519 ◽  
Author(s):  
J. G. Chen ◽  
A. B. Strawbridge ◽  
S. A. Kempson
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Time Course ◽  
Serum Starvation ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
System A ◽  
Microtubule Disruption ◽  
Stimulation Of

This study has focused on the possible influence of microtubules for the regulation of Na(+)-dependent system A neutral amino acid transport in A10 cells, a cultured cell line derived from rat aortic vascular smooth muscle. When microtubules were disrupted by incubating cells for 5 h in serum-free medium containing colchicine, nocodazole, or vinblastine, there was a twofold increase in system A transport (Vmax change). The dose for the disruption of microtubules by colchicine was similar to the dose required for the stimulation of system A. The time course showed that system A stimulation did not occur until widespread disruption of microtubules was established. The stimulation was specific for system A; there were no changes in glucose transport and Na(+)-dependent transport of phosphate and glutamate. Serum refeeding of quiescent cells from 2 days of serum starvation led to stimulation of system A, glucose, and phosphate transport. However, only system A was activated when colchicine was added to the serum-free medium. Addition of colchicine during serum refeeding had no additive effect for the stimulation of system A. The stimulation by both colchicine and serum was blocked by cycloheximide and actinomycin D. These findings suggest that microtubule disruption may activate system A gene expression.

Effect of Na-K adenosinetriphosphatase activity on relaxation of canine tracheal smooth muscle

1988 ◽  
Vol 64 (2) ◽  
pp. 635-641 ◽  
Author(s):  
S. J. Gunst ◽  
J. Q. Stropp
Keyword(s):  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Atpase Activity ◽  
Prostaglandin E2 ◽  
Sodium Nitroprusside ◽  
Tracheal Smooth Muscle ◽  
Free Medium ◽  
Inhibitory Effects ◽  
Ca2 Channels ◽  
Stimulation Of

The effect of Na-K adenosinetriphosphatase (ATPase) on relaxation induced by isoproterenol, prostaglandin E2, sodium nitroprusside, and forskolin, a specific stimulant of adenylate cyclase, was investigated in canine tracheal smooth muscle strips. Relaxation in response to isoproterenol, prostaglandin E2, and forskolin was significantly decreased after inhibition of the Na-K ATPase by ouabain or a potassium-free medium, but relaxation to sodium nitroprusside was not affected. Relaxation to isoproterenol was greater in muscles contracted by 5-hydroxytryptamine than in those contracted by acetylcholine. The stimulation of Na-K ATPase activity with potassium also caused differences in relaxation between tissues contracted with 5-hydroxytryptamine or acetylcholine. Relaxation caused by isoproterenol by activation of the Na-K-ATPase was also decreased by the Ca2+-channel antagonists, verapamil and diltiazem. The results suggest 1) Na-K ATPase activity modulates relaxation caused by isoproterenol, prostaglandin E2, and forskolin in canine tracheal smooth muscle, 2) isoproterenol or activation of the Na-K ATPase may cause relaxation partly by reducing Ca2+ influx through potential-dependent Ca2+ channels, and 3) the differences in the inhibitory effects of isoproterenol and Na-K ATPase activity on muscles contracted by acetylcholine and 5-hydroxytryptamine could be due to differences between these contractile agents in their dependence on extracellular Ca2+ for activation.

Evidence for an electrogenic sodium pump in smooth muscle

Life Sciences ◽  
1969 ◽  
Vol 8 (13) ◽  
pp. 769-773 ◽  
Author(s):  
G.S. Taylor ◽  
D.M. Paton ◽  
E.E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Sodium Pump ◽  
Electrogenic Sodium Pump

Cholinergic IPSP by Stimulation of the Electrogenic Sodium Pump

Nature ◽  
1969 ◽  
Vol 223 (5208) ◽  
pp. 864-865 ◽  
Author(s):  
G. A. KERKUT ◽  
L. C. BROWN ◽  
R. J. WALKER
Keyword(s):  
Sodium Pump ◽  
Electrogenic Sodium Pump ◽  
Stimulation Of

Alteration of Contractile Response of Artery Strips by a Potassium-Free Solution, Cardiac Glycosides and Changes in Stimulation Frequency

1957 ◽  
Vol 189 (1) ◽  
pp. 185-190 ◽  
Author(s):  
Edward Leonard
Keyword(s):  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Cardiac Glycosides ◽  
Contractile Response ◽  
Initial Period ◽  
Repetitive Stimulation ◽  
Free Medium ◽  
Relaxation Cycle ◽  
Time Required ◽  
Stimulation Of

Electrical stimulation of helically cut strips of rabbit carotid artery, mounted so as to allow development of tension isometrically, causes a contraction-relaxation cycle which remains reproducible for many hours, after an initial period of rising contractile response. If the strip is equilibrated in a potassium-free Krebs solution, or if a cardiac glycoside is added, the tension developed on electrical stimulation increases, the time required for relaxation is prolonged and contracture may also be observed. Desoxycorticosterone or progesterone decrease the contractile response of the strip. The arterial smooth muscle strip also exhibits the staircase phenomenon, a stepwise increase in tension on repeated stimulation after a period of rest. It is suggested that the changes in contractile response induced by a potassium-free medium, addition of glycosides, or repetitive stimulation are related to a loss of muscle fiber potassium. The action of the glycosides on the artery strip is discussed from the viewpoint of a model mechanism for altering vascular smooth muscle activity by affecting intracellular electrolytes.

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