196,123 research outputs found
Relation between Na+-K+ pump, Na+ activity and force in strophanthidin inotropy in sheep cardiac Purkinje fibres
No full textThe role of intracellular sodium activity in the inotropy potentiation among high [Ca]0 norepinephrine and strophanthidin
No full textRole of intracellular Na+ activity in the negative inotropy of strophanthidin in cardiac Purkinje fibers.
No full textCharacterization of the slowly inactivating sodium current INa2 in canine cardiac single Purkinje cells
No full textThe aim of our experiments was to investigate by means of a whole cell patch-clamp technique
the characteristics of the slowly inactivating sodium current (INa2) found in the plateau range
in canine cardiac Purkinje single cells. The INa2 was separated from the fast-activating and
-inactivating INa (labelledhere INa1)by applying a two-step protocol.Thefirst step, froma holding
potential (Vh) of −90 or −80 mV to −50 mV, led to the quick activation and inactivation of
INa1. The second step consisted of depolarizations of increasing amplitude from−50 mV to less
negative values, which led to the quick activation and slow inactivation of INa2. The INa2 was
fittedwith a double exponential functionwith time constants of tens and hundreds milliseconds,
respectively. After the activation and inactivation of INa1 at−50 mV, the slope conductance was
very small and did not change with time. Instead, during INa2, the slope conductance was larger
and decreased as a function of time. Progressively longer conditioning steps at−50 mVresulted
in a progressive decrease in amplitude of INa2 during the subsequent test steps. Gradually longer
hyperpolarizing steps (increments of 100 ms up to 600 ms) from Vh −30 mV to −100 mV
were followed on return to −30 mV by a progressively larger INa2, as were gradually more
negative 500 ms steps from Vh −30 mV to−90 mV. At the end of a ramp to−20 mV, a sudden
repolarization to approximately−35 mV fully deactivated INa2. The INa2 was markedly reduced
by lignocaine (lidocaine) and by low extracellular [Na+], but it was little affected by low and
high extracellular [Ca2+]. At negative potentials, the results indicate that there was little overlap
between INa2 and the transient outward current, Ito, as well as the calcium current, ICa. In
the absence of Ito and ICa (blocked by means of 4-aminopyridine and nickel, respectively),
INa2 reversed at 60mV. In conclusion, INa2 is a sodium current that can be initiated after the
inactivation of INa1 and has characteristics that are quite distinct from those of INa1. The results
have a bearing on the mechanisms underlying the long plateau of Purkinje cell action potential
and its modifications in different physiological and pathological conditions
Strophanthidin and force regulation by intracellular sodium activity in cardiac Purkinje fibers.
No full textRole of Intracellular Sodium Activity in the Control of Contraction in Cardiac Purkinje Fibers.
No full textThe role of intracellular sodium activity in the inotropy potentiation among high calcium, norepinephrine and strophanthidin
No full textIntracellular sodium activity and strophanthidin inotropy under conditions that vary cellular sodium
No full text
A slowly inactivating sodium current (INa2) in the plateau range in canine cardiac purkinje single cells.
No full textThe action potential of Purkinje fibres is markedly shortened by tetrodotoxin, suggesting the
possibility that a slowly inactivating sodium current might flow during the plateau. The aim of
the present experiments was to investigate, in canine cardiac Purkinje single cells by means of a
whole cell patch clamp technique, whether a sodium current slowly inactivates at less negative
potentials and (if so) some of its distinctive characteristics. The results showed that a 500 ms
depolarizing step from a holding potential of −90 mV to −50 mV induced the fast inward
current INa (labelled here INa1).With steps to−40 mV or less negative values, a slowly decaying
component (tentatively labelled here INa2) appeared, which peaked at −30 to −20 mV and
decayed slowly and incompletely during the 500 ms steps. The INa2 was present also during steps
to −10 mV, but then the transient outward current (Ito) appeared.When the holding potential
(Vh) was decreased to−60 to−50 mV, INa2 disappeared even if a small INa1 might still be present.
Tetrodotoxin (30 μM), lignocaine (100 μM) and cadmium (0.2mM; but not manganese, 1mM)
blocked INa2. During fast depolarizing ramps, the rapid inactivation of INa1 was followed by a
negative slope region. During repolarizing ramps, a region of positive slope was present,whereas
INa1 was absent. At less negative values of Vh, the amplitude of the negative and positive slopes
became gradually smaller.Gradually faster ramps increased the magnitude of the negative slope,
and tetrodotoxin (30 μM) reduced or abolished it. Thus, Purkinje cells have a slowly decaying
inward current owing to Na+ entry (INa2) that is different in several ways from the fast INa1 and
that appears important for the duration of the plateau
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