scholarly journals Cat Heart Muscle in Vitro

1962 ◽  
Vol 46 (2) ◽  
pp. 189-199 ◽  
Author(s):  
Ernest Page

The steady state transmembrane resting potential difference (Vm) has been measured in quiescent papillary muscles. Vm was determined as a function of the external K concentration in Cl and SO4 solutions and compared with the K equilibrium potential. Other measurements were made after replacement of external Na by choline, K by Rb and Cs, and Cl by SO4, CH3SO4, and NO3. Effects on Vm of albumin, temperature, and variation in internal K concentration are described.

1965 ◽  
Vol 48 (5) ◽  
pp. 933-948 ◽  
Author(s):  
Jon Goerke ◽  
Ernest Page

The exchange of cell K with K42, JK, has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. JK increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, PK, calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. JK is not affected by replacement of O2 by N2, or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10-5 M and 10-8 M ouabain.


1965 ◽  
Vol 48 (5) ◽  
pp. 949-956 ◽  
Author(s):  
Ernest Page

In quiescent cat papillary muscles JK, the rate of exchange of cellular K with K42 in the steady state, has been measured in the presence and absence of NaCl over a wide range of temperatures. JK was found to be independent of the presence of external NaCl under the steady state conditions investigated. The Arrhenius plot for K exchange was linear over a range of temperatures from 2.5 to 37.5°C in the absence of NaCl, and from 17.5 to 37.5°C in the presence of NaCl. The corresponding apparent activation energies were, respectively, 10,200 and 8,800 calories/mole. JK in the absence of NaCl was not affected by 10-5 M ouabain. These results are consistent with a passive distribution for the K of heart muscle cells. The observations suggest that a carrier-mediated forced exchange of K for Na does not occur during the steady state in mammalian heart muscle.


1960 ◽  
Vol 44 (2) ◽  
pp. 327-344 ◽  
Author(s):  
Ernest Page ◽  
A. K. Solomon

Methods have been developed for the simultaneous determination of total water, inulin space, and K and Na content in muscles of 0.5 to 10 mg. wet weight. These methods have been used to define steady state conditions with respect to intracellular K concentration in papillary muscles from cat hearts perfused and contracting isometrically at 27–28°C. and at 37–38°C. Cell volumes and intracellular ionic concentrations have been followed as a function of the external K concentration and compared with values predicted on the basis of electroneutrality and osmotic equilibrium.


1997 ◽  
Vol 77 (6) ◽  
pp. 2910-2924 ◽  
Author(s):  
C. F. Hsiao ◽  
P. R. Trueblood ◽  
M. S. Levine ◽  
S. H. Chandler

Hsiao, C. F., P. R. Trueblood, M. S. Levine, and S. H. Chandler. Multiple effects of serotonin on membrane properties of trigeminal motoneurons in vitro. J. Neurophysiol. 77: 2910–2924, 1997. Intracellular recordings from guinea pig trigeminal motoneurons (TMNs) in brain stem slices were used to determine the underlying ionic mechanisms responsible for our previously demonstrated enhancement of TMN excitability during jaw movements by serotonin (5-HT). 5-HT (0.5–100 μM) depolarized motoneurons and increased input resistance in the majority of neurons tested. Additionally, 5-HT reduced the amplitude of the postspike medium-duration afterhyperpolarization, decreased the current threshold for maintained spike discharge, and increased the maximum slope of the steady-state spike frequency-current relationship. Under voltage clamp, from holding potentials close to resting potential, 5-HT produced an inward current and a decrease in instantaneous slope conductance, suggesting a reduction in a resting K+ leak conductance ( I leak). The instantaneous current-voltage ( I-V) relationship for the inward 5-HT current ( I 5-HT) was linear throughout most of the voltage range tested. However, the steady-state I-V relationship showed some degree of inward rectification at potentials starting around −70 mV. The mean reversal potential for the instantaneous I 5-HT was −86.2 ± 4.5 (SE) mV ( n = 9), a value slightly negative to the predicted potassium equilibrium potential of −82 mV in these neurons. In the presence of 2 mM Ba2+, 5-HT application did not produce a further reduction in input conductance, but did expose a Ba2+-insensitive residual inward current that was resistant to Cs+ application. The instantaneous I-V relationship during 5-HT application in the presence of Ba2+ was shifted downward and parallel to control, suggesting that Ba2+ and 5-HT block the same resting I leak. The residual Ba2+- and Cs+-insensitive component of the total inward I 5-HT was voltage independent and was blocked when the extracellular Na+ was replaced by choline, suggesting that the predominant charge carrier for this residual current is Na+. 5-HT enhanced a hyperpolarization-activated cationic current, I h. In the presence of Ba2+, the time course of I 5-HT resembled that of I h and showed a similar voltage dependence that was blocked by extracellular Cs+ (1–3 mM). The effects of 5-HT on membrane potential, input resistance, and I h were partially mimicked by 5-HT2 agonists and suppressed by 5-HT2 antagonists. It is concluded that 5-HT enhances TMN membrane excitability through modulation of multiple intrinsic membrane conductances. This provides for a mechanism(s) to fine tune the input-output discharge properties of these neurons, thus providing them with greater flexibility in output in response to time-varying synaptic inputs during various movements of the jaw.


1966 ◽  
Vol 49 (4) ◽  
pp. 641-653 ◽  
Author(s):  
Ernest Page ◽  
S. R. Storm

Cell contents of water, K, Na, and Cl have been determined in cat right ventricular papillary muscles immersed in solutions with and without NaCl when the external osmolality was varied with sucrose. The plot of cell water/kilogram dry weight (corrected for sucrose content) vs. (external osmolality)-1 suggests that not less than 82% of water present in cells at physiological external osmolality is free to move across the cell membrane in response to an imposed osmotic gradient. Cells fail to increase their water content in very hypotonic solutions. For osmolalities greater than 5 times isosmolal, at which the mannitol space and the Cl36 space are both equal to 100% of muscle water, rather large amounts of univalent cation appear to remain "bound" to the tissue.


1995 ◽  
Vol 268 (6) ◽  
pp. F1148-F1153 ◽  
Author(s):  
N. Takahashi ◽  
Y. Kondo ◽  
O. Ito ◽  
Y. Igarashi ◽  
K. Omata ◽  
...  

Intracellular calcium plays an important role in the regulation of Cl- reabsorption in the ascending thin limb of Henle's loop (ATL). To elucidate the cytosolic Ca2+ dynamics in the ATL, intracellular Ca2+ concentration activity ([Ca2+]i) was measured in the in vitro microperfused hamster ATL using fura 2. Basal [Ca2+]i was 89.1 +/- 7.3 nM (n = 9 tubules). Removal of Ca2+ from the peritubular solution decreased [Ca2+]i from 89.1 +/- 7.3 to 64.1 +/- 7.1 nM in 2 min (n = 9, P < 0.05), whereas [Ca2+]i did not change after removal of Ca2+ from the luminal solution. Addition of 1 mM NaCN to the bath increased [Ca2+]i. This effect was completely abolished by the elimination of ambient Ca2+. Trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) in the bath reversibly increased [Ca2+]i, whereas addition of 1 mM ouabain to the bath decreased [Ca2+]i. Rates of changes in [Ca2+]i after removal and replacement of basolateral Ca2+ were not affected by removal of Na+, K+, or Cl- from the bath, whereas nicardipine decreased these parameters. Increasing bath K+ from 5 to 100 mM decreased [Ca2+]i from 69.3 +/- 5.8 to 50.8 +/- 5.0 nM in 1 min (n = 6, P < 0.05). Subsequent reduction of K+ from 100 to 5 mM increased [Ca2+]i to 174.0 +/- 30.8 nM in 1 min, followed by a gradual decrease in [Ca2+]i to a steady-state level of 74.2 +/- 8.0 nM in 2 min. Changes in basolateral K+ concentration did not affect [Ca2+]i in the absence of ambient Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)


1965 ◽  
Vol 208 (4) ◽  
pp. 770-775 ◽  
Author(s):  
Mario Vassalle

Transmembrane potentials were recorded from mammalian Purkinje fibers. Adding saccharose to the bathing solution slowed the spontaneous rate, probably as a result of cell shrinkage and an increase in the intracellular K concentration. An opposite result was found with hypotonic medium. In solutions containing 5.4 mm K the fibers were quiescent. Lowering K to 2.7 mm left the membrane resting potential unchanged but decreased the membrane conductance to half. There was only a minor effect of extracellular K on membrane conductance during the plateau of the action potential. Spontaneous firing regularly started when extracellular K was reduced to or below 2.7 mm. This was preceded by subthreshold oscillations which increased in amplitude. A low K conductance associated with a sizeable difference between membrane potential and potassium equilibrium potential seem to be essential for spontaneous activity to occur in cardiac tissue.


1987 ◽  
Vol 65 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti

The diffusion and electrogenic components of the resting potential of hypoxic ventricular muscle were separated by inhibition of the sodium pump with 10−4 M ouabain. The response to varying external K concentrations (Ko) was studied. Arteriaily perfused rabbit hearts were submitted to 60 min hypoxia in Krebs solution containing 5 mM K throughout or to different external K concentrations during the last 20 min of hypoxia. For K concentrations between 1.5 and 10 mM, hypoxia did not change the resting potential except for a slight hyperpolarization in 7.5 mM K. The diffusion component of the resting potential did not differ from the resting potential at Ko < 5 mM. An electrogenic potential of −3 to −6 mV was detectable at Ko values between 5 and 10 mM. The internal K concentration, Ki, was estimated from extrapolations to zero potential of the relation resting potential vs. Ko in normoxic and hypoxic hearts. These experiments revealed a decline of Ki of 16 mM with hypoxia. The variation of the diffusion potential with external K was fitted by a PNa:PK ratio five times lower than in normoxia. It has been concluded that an increase in K permeability and the persistence of electrogenic Na extrusion during hypoxia of rather short duration prevent membrane depolarization despite the myocardial K loss.


1964 ◽  
Vol 47 (3) ◽  
pp. 531-543 ◽  
Author(s):  
Ernest Page ◽  
R. J. Goerke ◽  
S. R. Storm

Cellular concentrations, [K]i, [Na]i, and [Cl]i, and cell water contents were measured in vitro at 27°C in cat papillary muscles. Measurements were made with and without ouabain at varying concentrations of K and ouabain, at pH 5.2 and 9.0, in absence of O2, and in NaCl-free solution. Large losses of cell K and increases of cell Na occurred in presence of ouabain, at 2–3°C, and in K-free medium. The dependence of inhibition of cation transport by ouabain on external K concentration, studied at constant initial [K]i, was consistent with a competition between K and ouabain localized to the external face of the membrane. In NaCl-free sucrose solution [K]i remained at its physiological value and was not affected by exposure to ouabain or low temperature, except when Ca was also omitted. Ouabain inhibition persisted at pH 9.0 and in Ca-poor media. Cells swelled and lost K at pH 5.2, and residual ouabain effect was small. At pH 9.0, or in absence of O2, or in Ca-poor solutions cells became permeable to mannitol. The ion movements observed after inhibition of active transport are compatible either with a passive K distribution and a primary inhibition of Na extrusion or with inhibition of a coupled active transport of both K and Na.


1995 ◽  
Vol 268 (6) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Y. K. Kim ◽  
W. H. Dantzler

We measured the effects of changes in bath K+ concentration ([K+]) on basolateral membrane potential difference (PD) and [3H]tetraethylammonium (TEA) transport in isolated snake (Thamnophis) proximal renal tubules (25 degrees C; pH 7.4). Increasing bath [K+] from 3 to 65 mM decreased PD from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA by approximately 25%, indicating that PD influences TEA entry into the cells. Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by unlabeled TEA, indicating that uptake is carrier mediated. Kt (approximately 18 microM) for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM K+, suggesting that the decrease in PD or the increase in [K+] alters the affinity of the transporter for TEA. The steady-state cell-to-bath ratio for [3H]TEA with 3 mM K+ (-60 mV PD) was approximately 16, significantly above the ratio of 10 predicted for passive distribution at electrochemical equilibrium. With 65 mM K+ (-20 mV PD) this ratio decreased to approximately 6, again significantly above the predicted ratio of 2. These data suggest that the PD can account for much, but not all, of the steady-state uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was identical with either 3 or 65 mM K+ in the bath but was almost completely inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA uptake. These data indicate that virtually all TEA transport across the basolateral membrane is carrier mediated and that transport out of the cells is unaffected by PD.


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