Factors related to the low resting membrane potentials of diseased human atrial muscles.

Imanishi, Sunao; Arita, Makoto

doi:10.2170/jjphysiol.37.393

Cited by 22 publications

(20 citation statements)

References 30 publications

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“…This finding was not expected and has not heretofore been reported. It is interesting to speculate that severe stretches increased gK1 and resulted in hyperpolarization, since 1) the hyperpolarization occurred predominantly in relatively lower [K+]0 in which gK1 is expected to be low (KAMEYAMA et al, 1983), and 2) the direction of changes in the RP-[K+]0 relationship produced by a severe stretch was just opposite to that reported in the case of atrial muscles having decreased gK1 (IMANISHI and ARITA, 1987). The hyperpolarization may not be due to the increase in [K+]; or increased equilibrium potential for K+, because 3 curves in Fig.…”

Section: Discussionmentioning

confidence: 87%

Effects of mechanical stretch on the membrane potential of guinea pig ventricular muscles.

et al. 1988

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We studied the effect of stretch on the membrane potentials and ultrastructure of isolated ventricular papillary muscles of guinea pigs. The muscles were stimulated at 0.5 Hz and stretched stepwise from slack length (90% of Lmax) to 100% (mild stretch), 110-120% (moderate stretch), and 130-140% of Lmax (severe stretch), under microscopic control. In control Tyrode solution (K + = 5.4 mM, Ca2 + =1.8 mM, Mg2 + = 0.5 mM), the mild to moderate stretch significantly depolarized the resting potential (RP) by about 6 mV as compared to that in slack length, whereas the severe stretch hyperpolarized the membrane by about 5 mV. The latter finding was new and was focused on in later experiments. Both the hyperpolarization and depolarization became more marked when [K+]0 was decreased to 1.35-2.7 mM, and became less with elevated [K+]o to 10.8--21.6 mM, thereby suggesting the participation of altered K+ conductance (gK) with these changes in the RP. Perfusion with low [Ca2 +]o (0.45 mM) enhanced the depolarization but eliminated the hyperpolarization; high [Ca2 +]o (7.2 mM) inhibited the depolarization without effect on the hyperpolarization. D-600 (1 /IM), caffeine (10 mM), and ryanodine (1 µM), all of which may produce decreases in [Ca2 +]i, abolished the hyperpolarization with inconsistent effects on the depolarization. Moderate to severe stretches decreased the maximum rate of rise of action potential (Vmax)' by shifting the Vmax'M relationship toward hyperpolarizing direction. The shift could be reversed partially after increasing [Mg2 +]o to 8.0 mM. Electron microscopic examination revealed that the sarcoplasmic reticulum (SR) remained intact with mild to moderate stretches with significant lengthening of sarcomere length, while with a severe stretch, the SR showed a structural disarrangement with a non-uniform lengthening of sarcomere length. Our observations suggest that stretch-induced hyperpolarization is probably mediated by the increase in gK, presumably secondary to the increase in

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Section: Discussionmentioning

confidence: 87%

Effects of mechanical stretch on the membrane potential of guinea pig ventricular muscles.

et al. 1988

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“…The resting membrane potential of the right atrial muscle excised from the patients with congenital or acquired heart disease ("diseased atrial muscle") is generally decreased, probably due to chronic hemodynamic overload or ischemia that might have been imposed on the atrium for a long period of time (MARY-RABINE et al, 1983;LEE, 1986;IMANISHI and ARITA, 1987). In the present study using such "diseased right atrial muscles ," we measured aK and Vm in non-driven conditions and found the a K to be 99.7 + 1.3 mM and the Vm, -43.9±1.4 mY.…”

Section: Discussionmentioning

confidence: 99%

“…Diseased human atrial fibers are characterized by low, non-uniform levels of the resting membrane potential (TEN EICK and SINGER, 1979;MARY-RABINE et al, 1983;IMANISHI and ARITA, 1987). Such changes have been attributed to non-homogeneous decreases in the resting K+ conductance (TEN Elck and SINGER, 1979), increases in the resting Na + conductance (IMANISHI and ARITA, 1987), and impairment of the electrogenic Na-K pump (LEE, 1986).…”

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confidence: 99%

“…Such changes have been attributed to non-homogeneous decreases in the resting K+ conductance (TEN Elck and SINGER, 1979), increases in the resting Na + conductance (IMANISHI and ARITA, 1987), and impairment of the electrogenic Na-K pump (LEE, 1986). However, IMANISHI and ARITA (1987) emphasized the role of electrogenic Na-K pump current in maintaining the resting potential at relatively high levels, which counteracted the depolarization due to the altered ionic membrane conductance. However, their conclusion was derived from alterations of the membrane potential measured before and after inhibition of the Na-K pump by various procedures such as ouabain or low external K + concentration, which inevitably affects the membrane conductance.…”

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confidence: 99%

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Unaffected electrogenic Na-K pump activity in "diseased" human atrial fibers, as assessed by intracellular K+ activity.

Sako

Imanishi²,

Arita

et al. 1989

Jpn.J.Physiol

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To investigate the role of the electrogenic Na-K pump in the resting membrane of "diseased" or "depolarized" human atrial muscles, intracellular K+ activity (ak) and resting membrane potential (Vm) were simultaneously measured using double-barreled K+-selective microelectrodes. Under perfusion with normal Tyrode's solution (37°C) containing 5.4 mM [K]0, Vm averaged -43.9 + 1.4 mV, and aK was 99.7 + 1.3 mM (mean + S.E., n = 33). The aK was comparable to that of atrial muscles obtained from other intact mammalian species. In 5.4 mM [K]0, dihydro-ouabain (DHO) at concentrations of 10 -6 and 10 -5 M significantly decreased aK and depolarized Vm. Similar decreases in aK were observed when [K]0 was decreased from 5.4 to 0.5 mM or when the temperature of the perfusing solution was decreased from 37 to 22°C. Upon returning [K]0 from 0.5 to 5.4 mM at 37°C, aK increased, Vm hyperpolarized markedly for about 3 min, and this was followed by less marked levels of hyperpolarization in the steady state. The high [K]0-induced increases in aK were inhibited in the presence of DHO, and at low temperature (22°C). Isoproterenol (10-' M) increased aK and hyperpolarized Vm. Acetylcholine (10 -5M) hyperpolarized Vm with no change in aK. The rate of reduction of Na+-efflux during application of DHO (10 -5 M) was calculated based on the change in aK and surface-to-volume ratio of the cell measured electronmicroscopically in the same tissue, and estimated to be 2.6 to 3.8 pmol/(cm2 . s), close to the value reported for Purkinje fibers excised from intact animals. We conclude that the Na-K pump functions normally even in "diseased" human atrial muscles, thereby keeping aK within a physiological range.

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“…These findings support the notion that activation of 'Ca contributes to the pacemaker potential of the slow-type AAPs. However, it must be remembered that in diseased human atrial muscles, the resting potassium conductance (gK,) is generally decreased, and the resting sodium conductance considerably increased (IMANISHI and ARITA, 1987). Such conditions are responsible for the low resting potential of these preparations and certainly favour the development of both "slow-" and "fast-"type AAPs.…”

Section: Discussionmentioning

confidence: 99%

Two differential mechanisms of automaticity in diseased human atrial fibers.

et al. 1988

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The ionic mechanisms of automaticity in spontaneously active preparations (n = 38) from "diseased" human atria were investigated. The cycle length (CL) of the automatic action potential (AAP) ranged from 0.6 to 4.5 s (mean + S.D.: 2.0 + 1.0 s). The AAP from preparations obtained from non-digitalized patients (group 1, n = 29) showed various CLs, in that 16 patients had a CL longer than 2.0 s (slow-type AAP) while in tissues from the other 13 patients, the CL was 2.0 s or less (fast-type AAP). On the other hand, all preparations obtained from the digitalized patients prior to cardiac surgery (group 2, n = 9) had the fast-type AAP (CL <_ 2.0 s). The slow-type AAP was accelerated and changed to the fast one after application of ouabain (1 µM) or by perfusing with 50% [Na + ]o Tyrode solution. Ryanodine (1 tiM), a specific inhibitor of calcium release from the sarcoplasmic reticulum (SR), markedly lengthened the CL of fast-type AAP, without affecting the slow-type AAP. In contrast, caffeine (15 mM) shortened the CL of the slow-type AAP and remarkably lengthened the CL of the fast-type AAP, as is the case in ryanodine. The rate of slow-type AAP was enhanced with an increase in [Ca2+]o and depressed with a decrease in [Ca2 +]o or with application of diltiazem, a Ca2 + channel blocker. The slow-type AAP was changed to the fast-type AAP by stretching the preparation by about 20%. In vitro preparations excised from patients with dilated atria revealed a shorter CL of AAPs. We conclude that in "diseased" human atrial preparations, the ionic mechanism responsible for generation of slow-and fast-type automaticity differs. Slow automaticity (CL >2.0 s) perhaps relates to activation of the slow inward Ca2 + current, while the fast-type automaticity (CL <2.0 s) is linked to cyclic increases in [Ca2 +]~.

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Factors related to the low resting membrane potentials of diseased human atrial muscles.

Cited by 22 publications

References 30 publications

Effects of mechanical stretch on the membrane potential of guinea pig ventricular muscles.

Effects of mechanical stretch on the membrane potential of guinea pig ventricular muscles.

Unaffected electrogenic Na-K pump activity in "diseased" human atrial fibers, as assessed by intracellular K+ activity.

Two differential mechanisms of automaticity in diseased human atrial fibers.

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