Mechanism of Inhibition of Smooth Muscle Tension in Guinea-Pig Taenia Coli by Ouabain

1974 ◽  
Vol 52 (4) ◽  
pp. 898-901 ◽  
Author(s):  
D. Bose
Keyword(s):  
Guinea Pig ◽  
Muscle Tension ◽  
Sodium Concentration ◽  
Inhibitory Response ◽  
The Other ◽  
Extracellular Potassium ◽  
Taenia Coli ◽  
Mechanism Of Inhibition ◽  
Intracellular Sodium Concentration ◽  
Extracellular Sodium

Ouabain produced an increase in tension in the guinea-pig taenia coli which was abolished in the presence of high extracellular potassium. On the other hand the delayed inhibitory response of ouabain could only be abolished by the removal of extracellular sodium. The mechanism of inhibition of contraction by ouabain appears to be due to elevation of intracellular sodium concentration.

Sodium dependence of carnitine transport in isolated perfused adult rat hearts

1983 ◽  
Vol 244 (2) ◽  
pp. H247-H252 ◽  
Author(s):  
T. C. Vary ◽  
J. R. Neely
Keyword(s):  
Potassium Concentration ◽  
Sodium Concentration ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration ◽  
Rat Hearts ◽  
Carrier Mediated Transport ◽  
Physiological Serum ◽  
Carnitine Transport ◽  
Extracellular Sodium ◽  
Carnitine Concentration

In heart muscle, the intracellular carnitine concentration is approximately 40 times higher than the plasma carnitine concentration, suggesting the existence of an active transport process. At physiological serum carnitine concentrations (44 microM), 80% of total myocardial carnitine uptake occurs via a carrier-mediated transport system. The mechanism of this carrier-mediated transport was studied in isolated perfused rat hearts. Carnitine transport showed an absolute dependence on the extracellular sodium concentration. The rate of carnitine transport was linearly related to the perfusate sodium concentration at every perfusate carnitine concentration examined (15-100 microM). Total removal of extracellular sodium completely abolished the carrier-mediated transport. Decreasing the perfusate potassium concentration from a control of 5.9 to 0.6 mM stimulated transport by 35%, whereas increasing the extracellular potassium concentration from 5.9 to 25 mM reduced transport by 60%. The carrier-mediated transport was inversely proportional to the extracellular potassium concentration. Acetylcholine (10(-3) M), isoproterenol (10(-7) M), or ouabain (10(-3) did not alter the rate of carnitine transport. Addition of tetrodotoxin (10(-5) stimulated carnitine transport by about 40%, while gramicidin S (5 X 10(-6) M) decreased uptake by about 18% relative to control. The data provide evidence that carnitine transport by cardiac cells occurs by a Na+-dependent cotransport mechanism that is dependent on the Na+ electrochemical gradient.

scholarly journals The Ionic Basis of Electrical Activity in Embryonic Cardiac Muscle

1968 ◽  
Vol 52 (3) ◽  
pp. 666-681 ◽  
Author(s):  
Billy K. Yeh ◽  
Brian F. Hoffman
Keyword(s):  
Electrical Activity ◽  
Sodium Concentration ◽  
Cardiac Cells ◽  
Resting Potential ◽  
Extracellular Potassium ◽  
Embryonic Chick ◽  
Extracellular Potassium Concentration ◽  
Chick Heart ◽  
Extracellular Sodium ◽  
Ionic Basis

The intracellular sodium concentration reported for young, embryonic chick hearts is extremely high and decreases progressively throughout the embryonic period, reaching a value of 43 mM immediately before hatching. This observation suggested that the ionic basis for excitation in embryonic chick heart may differ from that responsible for electrical activity of the adult organ. This hypothesis was tested by recording transmembrane resting and action potentials on hearts isolated from 6-day and 19-day chick embryos and varying the extracellular sodium and potassium concentrations. The results show that for both young and old embryonic cardiac cells the resting potential depends primarily on the extracellular potassium concentration and the amplitude and rate of rise of the action potential depend primarily on the extracellular sodium concentration.

Mechanism of inhibition of contraction by cadmium in guinea-pig taenia coli

1983 ◽  
Vol 35 (8) ◽  
pp. 505-510 ◽  
Author(s):  
T. NASU ◽  
H. KOSHIBA ◽  
K. MASE ◽  
Y. ISHIDA
Keyword(s):  
Guinea Pig ◽  
Taenia Coli ◽  
Mechanism Of Inhibition

scholarly journals The Ionic Basis of Electrical Activity in Embryonic Cardiac Muscle

1968 ◽  
Vol 52 (4) ◽  
pp. 666-681 ◽  
Author(s):  
Billy K. Yeh ◽  
Brian F. Hoffman
Keyword(s):  
Electrical Activity ◽  
Sodium Concentration ◽  
Cardiac Cells ◽  
Resting Potential ◽  
Extracellular Potassium ◽  
Embryonic Chick ◽  
Extracellular Potassium Concentration ◽  
Chick Heart ◽  
Extracellular Sodium ◽  
Ionic Basis

The intracellular sodium concentration reported for young, embryonic chick hearts is extremely high and decreases progressively throughout the embryonic period, reaching a value of 43 mM immediately before hatching. This observation suggested that the ionic basis for excitation in embryonic chick heart may differ from that responsible for electrical activity of the adult organ. This hypothesis was tested by recording transmembrane resting and action potentials on hearts isolated from 6-day and 19-day chick embryos and varying the extracellular sodium and potassium concentrations. The results show that for both young and old embryonic cardiac cells the resting potential depends primarily on the extracellular potassium concentration and the amplitude and rate of rise of the action potential depend primarily on the extracellular sodium concentration.

Plasma membrane Na(+)-H+ antiporter and H(+)-ATPase in the medullary thick ascending limb of rat kidney

1992 ◽  
Vol 262 (4) ◽  
pp. C963-C970 ◽  
Author(s):  
M. Froissart ◽  
P. Borensztein ◽  
P. Houillier ◽  
F. Leviel ◽  
J. Poggioli ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Sodium Concentration ◽  
Iodoacetic Acid ◽  
Extracellular Potassium ◽  
Thick Ascending Limb ◽  
Bafilomycin A1 ◽  
Inhibitory Effects ◽  
Medullary Thick Ascending Limb ◽  
Ethanesulfonic Acid ◽  
Extracellular Sodium

To characterize H+ transport mechanisms in a fresh suspension of rat medullary thick ascending limb (MTAL) tubules, we have monitored intracellular pH (pHi) with use of the fluorescent probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. First, a Na(+)-H+ antiporter was identified in bicarbonate-free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered media at 25 degrees C. pHi recovery of Na-depleted acidified cells was dependent on extracellular sodium concentration, which was inhibited by amiloride in a manner consistent with simple competitive interaction with one external transport site (amiloride Ki = 1.5-2.1 x 10(-5) M); Na-induced pHi recovery of acidified cells was electroneutral since it was not affected by 5 or 100 mM extracellular potassium in the presence or absence of valinomycin. Second, at 37 degrees C, pHi recovery after acute intracellular acidification caused by 40 mM acetate addition to cell suspension was inhibited 36% by 200-400 nM bafilomycin A1, a macrolide antibiotic that specifically inhibits vacuolar-type H(+)-ATPase at submicromolar concentrations. In addition, amiloride-insensitive pHi recovery was inhibited by bafilomycin A1, 10(-3) M N-ethylmaleimide, and 10(-4) M preactivated omeprazole but not by 10(-5) M vanadate, 10(-4) M SCH 28080, or removal of extracellular potassium. Also, metabolic inhibition by absence of substrate, 10(-4) M KCN, or 5 x 10(-4) M iodoacetic acid inhibited amiloride-insensitive pHi recovery. The inhibitory effects of absence of metabolic substrate and iodoacetic acid were removed by reexposure to glucose and L-leucine and by exogenous ATP, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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