Role of Intracellular Sodium Activity in the Control of Contraction in Cardiac Purkinje Fibers

1994 ◽  
Vol 1 (1) ◽  
pp. 28-42 ◽  
Author(s):  
P. Abete ◽  
M. Vassalle
Keyword(s):  
Intracellular Sodium ◽  
Purkinje Fibers ◽  
Sodium Activity ◽  
Cardiac Purkinje Fibers

Acetylcholine increases intracellular sodium activity in sheep cardiac Purkinje fibers

1989 ◽  
Vol 256 (5) ◽  
pp. H1407-H1416
Author(s):  
G. Iacono ◽  
M. Vassalle
Keyword(s):  
Action Potential ◽  
Spontaneous Activity ◽  
Sodium Pump ◽  
Contractile Force ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Sodium Activity ◽  
Cardiac Purkinje Fibers

The action of acetylcholine (ACh) on intracellular sodium activity (alpha iNa) was studied in sheep Purkinje fibers by means of a Na+-selective microelectrode technique while transmembrane potentials and contractile force were simultaneously recorded. In quiescent fibers, 10(-4) to 10(-5) M ACh shifted the resting potential to less negative values and increased alpha iNa from 5.57 +/- 0.21 to 6.45 +/- 0.35 mM (+15.8%, P less than 0.005). In other experiments, ACh induced a depolarization that initiated spontaneous activity. In fibers driven at 60 beats/min, ACh prolonged the action potential, increased alpha iNa from 7.98 +/- 0.15 to 9.36 +/- 0.3 mM (+17.29%, P less than 0.005), and increased contractile force. Norepinephrine (10(-5) to 10(-6) M) increased contractile force and decreased alpha iNa, but in its presence ACh still increased force and alpha iNa and vice versa. Strophanthidin (10(-4) M) increased alpha iNa, and 3 x 10(-6) M propranolol and 10(-6) M atropine decreased alpha iNa. Both strophanthidin and atropine (but not propranolol) prevented the increase in alpha iNa by ACh. It is concluded that the ACh increases alpha iNa and contractile force through the inhibition of the sodium pump and that these actions are due to the activation of the muscarinic receptor and not to endogenously released norepinephrine.

The interrelationship of cesium, intracellular sodium activity, and pacemaker potential in cardiac Purkinje fibers

1990 ◽  
Vol 68 (9) ◽  
pp. 1236-1246 ◽  
Author(s):  
Giovanni Iacono ◽  
Mario Vassalle
Keyword(s):  
Membrane Potential ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Sodium Activity ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Myocardial Fibers

The actions of cesium (Cs) on intracellular sodium activity [Formula: see text], membrane potentials, and force were studied in sheep cardiac Purkinje and myocardial fibers superfused in vitro. In Purkinje fibers, Cs (2 mM) decreased diastolic depolarization, [Formula: see text] (−6.7%, p < 0.005), and force (−28.0%, p < 0.01). The effects of 4 and 8 mM Cs were more pronounced. In quiescent fibers, Cs (2–4 mM) also decreased [Formula: see text] (−17.3%, p < 0.005) and induced an initial hyperpolarization (+5.6 ± 1.3%, p < 0.005) followed by a return toward control. Diastolic depolarization was almost abolished by driving the fibers at 180/min (diastole was very short) but still Cs decreased [Formula: see text] (−15.4%). Tetrodotoxin decreased [Formula: see text] (−16.2%, p < 0.025) and reduced the Cs-induced fall in [Formula: see text] (−2.2%, p < 0.05). In zero [K]o, Cs decreased [Formula: see text] and caused repolarization. In 0.1 mM strophanthidin, Cs did not decrease [Formula: see text] any longer and affected the membrane potential little. In quiescent myocardial fibers, Cs (4 mM) decreased [Formula: see text] (−12.6%, p < 0.05) and transiently hyperpolarized (+2.1%). Rubidium (2 mM) decreased [Formula: see text] and resting potential in Purkinje fibers and in myocardial fibers and also decreased diastolic depolarization in Purkinje fibers. Thus, cesium and rubidium decrease [Formula: see text] and modify the membrane potential but not through a block of the inward pacemaker current If.Key words: rubidium, intracellular sodium activity, diastolic depolarization, tetrodotoxin, strophanthidin.

Modulation of intracellular Na+ activity and cardiac force by norepinephrine and Ca2+

1983 ◽  
Vol 244 (1) ◽  
pp. C110-C114 ◽  
Author(s):  
C. O. Lee ◽  
M. Vassalle
Keyword(s):  
Contractile Force ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Purkinje Fibers ◽  
Intracellular Na Activity ◽  
Cardiac Purkinje Fibers ◽  
High Calcium ◽  
Ion Activity ◽  
Ion Activities ◽  
Stimulation Of

The actions of norepinephrine and high calcium on the electrical, mechanical, and intracellular sodium ion activities were studied in electrically driven canine cardiac Purkinje fibers under different conditions. It was found that norepinephrine and high calcium decrease intracellular sodium ion activity (aiNa). The exposure to either agent is followed by a transient decline of force that correlates with the lower aiNa. Inhibition of the Na+ -K+ pump by strophanthidin reduces or abolishes the decrease in aiNa by norepinephrine but not that by high calcium. It is concluded that norepinephrine and high calcium both decrease aiNa and thereby the contractile force but (unlike high calcium) norepinephrine acts through the stimulation of the Na+ -K+ pump.

Role of calcium and sodium in strophanthidin inotropy in cardiac Purkinje fibers

1981 ◽  
Vol 240 (4) ◽  
pp. H561-H570
Author(s):  
M. L. Bhattacharyya ◽  
M. Vassalle
Keyword(s):  
Inotropic Effect ◽  
Force Of Contraction ◽  
Tyrode Solution ◽  
Purkinje Fibers ◽  
Low Concentration ◽  
Cellular Calcium ◽  
Cardiac Purkinje Fibers ◽  
High Calcium

The effects of strophanthidin on electrical and mechanical events in canine cardiac Purkinje fibers were studied in vitro in the absence and presence of tetrodotoxin (TTX), norepinephrine, and high calcium. In Tyrode solution, strophanthidin (1-3 X 10(-7) M), norepinephrine (3-5 X 10(-7) M), and high calcium 8.1 mM) increased the force of contraction, and TTX markedly reduced it. In the presence of TTX, strophanthidin had little or no inotropic effect, whereas that of norepinephrine and high calcium was less than in Tyrode solution. In the presence of TTX, strophanthidin increased force markedly if (and as long as) either norepinephrine or high calcium were also present. A higher dose of strophanthidin (10(-6) M) induced a markedly delayed increase in force in presence of TTX. The results suggest that, in the presence of TTX, in a low concentration strophanthidin has little effect on force, because cellular calcium is low; however, it becomes effective when the calcium is increased by norepinephrine or high calcium. In toxic doses, strophanthidin increases force even in the presence of TTX as the inhibition of the pump should increase intracellular sodium and therefore calcium.

Role of calcium in caffeine-norepinephrine interactions in cardiac Purkinje fibers

1989 ◽  
Vol 257 (1) ◽  
pp. H226-H237 ◽  
Author(s):  
H. Satoh ◽  
M. Vassalle
Keyword(s):  
Calcium Concentration ◽  
Iodoacetic Acid ◽  
Slow Inward Current ◽  
Extracellular Potassium ◽  
Purkinje Fibers ◽  
Extracellular Potassium Concentration ◽  
Cardiac Purkinje Fibers ◽  
Ca Uptake

Caffeine-norepinephrine interactions were studied in canine cardiac Purkinje fibers perfused in vitro. Caffeine (0.5-1 mM) or theophylline (0.5-1 mM) increased and then decreased contractile force in the absence and presence of 0.5-10 microM norepinephrine (NE) [in high extracellular calcium concentration ([Ca]o) caffeine only decreases force]. Occasionally, caffeine only decreased force in the presence of NE. In the presence of NE and 12 mM (sometimes even 4 mM) extracellular potassium concentration, caffeine did not decrease force below the precaffeine level. Reciprocally, in 0.5-2 mM caffeine NE increased force, although less than in the absence of caffeine. Even in 9 mM caffeine, NE increased force but slowed the final phase three repolarization of the action potential. Both NE and 8.1 mM [Ca]o increased force, but NE decreased force in the presence of high [Ca]o. In NE and propranolol (or propranolol alone), caffeine only increased force, whereas it had the usual effects in the presence of methoxamine or phenotolamine. In the presence of iodoacetic acid and 2-deoxy-D-glucose, NE caused contracture and caffeine exaggerated it. In contrast, in NE and 2 mM Mn, caffeine only increased force. It is concluded that initially NE diminishes the cytoplasmic calcium overload induced by caffeine (by promoting Ca uptake into the sarcoplasmic reticulum) and subsequently enhances it (by increasing the slow inward current).

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