Effects of Ca2+ and catecholamines on the guinea pig atrium action potential plateau

1977 ◽  
Vol 233 (2) ◽  
pp. H203-H210
Author(s):  
R. B. Robinson ◽  
W. W. Sleator
Keyword(s):  
Guinea Pig ◽  
Calcium Concentration ◽  
Potassium Conductance ◽  
Slow Inward Current ◽  
Activation Process ◽  
Action Potential Plateau ◽  
Guinea Pig Atrium ◽  
Opposing Effects ◽  
Guinea Pig Atria ◽  
External Calcium

The activation process in isolated electrically driven guinea pig atria was studied by means of simultaneous microelectrode and tension recording. Reducing external calcium from 2.5 to 1.25 mM prolonged the plateau but further reduction of calcium shortened it. Progressively increasing doses of the calcium antagonist D600 (up to 1.4 micrometer), however, monotonically decreased plateau duration. Either protocol monotonically decreased steady-state tension, but with markedly different effects on the restitution relation. Epinephrine, and to a lesser extent isoproterenol, restored plateau duration after exposure to either a calcium-free or D600-containing solution, but only the isoproterenol effect was propranolol sensitive. Addition of calcium chelators enhanced rather than prevented the effect of epinephrine on plateau duration in a calcium-free solution, extending the plateau duration to more than 3 times normal in some cases. These results are explained in terms of two opposing effects of a change in calcium concentration on plateau formation, one action being through the slow inward current and the second through a shift in a calcium dependence of the inward-rectifying, potassium conductance system.

Ouabain uptake by endocytosis in isolated guinea pig atria

1988 ◽  
Vol 255 (4) ◽  
pp. C479-C485 ◽  
Author(s):  
H. Nunez-Duran ◽  
L. Riboni ◽  
E. Ubaldo ◽  
E. Kabela ◽  
L. Barcenas-Ruiz
Keyword(s):  
Electron Microscope ◽  
Guinea Pig ◽  
Mammalian Cells ◽  
Isometric Tension ◽  
Cardiac Cells ◽  
Inotropic Effect ◽  
Experimental Protocols ◽  
Guinea Pig Atrium ◽  
Endocytic Vesicles ◽  
Guinea Pig Atria

Mammalian cells specifically internalize some molecular species through receptor-mediated endocytosis (RME). We have used four different experimental protocols to investigate whether ouabain enters cardiac cells of guinea pig atrium through this pathway. First, by electron microscope morphometry we found that ouabain increased endocytic vesicles in atrial cells. Second, by scintillation counting we found that [3H]ouabain uptake by the tissue is decreased by three treatments that decrease RME, i.e., NH4Cl, trifluoperazine, and 16 mM [K+]0. Third, by radioautography at the electron microscope level, we checked that in preceding experiments [3H]ouabain was washed out of plasma membrane after 60-min rinse and interiorized into the cardiac cells. Fourth, isometric tension recordings showed that the positive inotropic effect of ouabain was diminished in the presence of inhibitors, whereas that of a hydrophobic analogue, ouabagenin, was not affected. These results suggest that ouabain enters cardiac cells through RME and also that an intracellular site may, at least in part, be responsible for its inotropic effect.

Negative inotropic effect of extracellular calcium buffering in cardiac muscle

1987 ◽  
Vol 252 (2) ◽  
pp. C248-C252 ◽  
Author(s):  
Y. Shimoni ◽  
S. Ginsburg
Keyword(s):  
Guinea Pig ◽  
Cardiac Muscle ◽  
Heart Muscle ◽  
Calcium Concentration ◽  
Negative Inotropic Effect ◽  
Intracellular Acidosis ◽  
Calcium Buffering ◽  
The Mean ◽  
Frog Atrium ◽  
External Calcium

Heart muscle contracts more vigorously when calcium levels are raised. A transient depletion of calcium from restricted extracellular spaces occurs with each contraction. We decided to maintain the concentration of this ion at a constant level by using an external calcium buffering system. It was found that buffering calcium at a millimolar level (using citrate as a buffer) caused a decrease, rather than an increase in the strength of contraction. The mean reduction in peak tension was by 27% in guinea pig and by 50.5% in frog atrium. This finding is analyzed; its most plausible explanation is the hypothesis that the buffer dissipates a calcium inhomogeneity, consisting of a higher calcium concentration adjacent to the membrane. Alternative interpretations such as intracellular acidosis, were tested experimentally and ruled out.

Effects of ouabain and calcium on potassium balance of isolated guinea pig ventricle

1962 ◽  
Vol 203 (6) ◽  
pp. 1130-1134 ◽  
Author(s):  
J. B. Kahn ◽  
Edwin Eakin ◽  
Don E. Levi
Keyword(s):  
Guinea Pig ◽  
Flow Rate ◽  
Binding Sites ◽  
Calcium Concentration ◽  
Ringer Solution ◽  
Potassium Balance ◽  
Anionic Binding Sites ◽  
External Calcium

Isolated guinea pig ventricles were perfused as follows: A—45 min with normal Krebs-Ringer solution containing tracer amounts of K42 (NKR*); B—15 min with NKR*, 15 min with KR* in which half the calcium was replaced with sodium (Ca/2-KR*), 15 min with NKR*; C—15 min with NKR*, 15 min with Ca/2-KR*, 15 min with Ca/2-KR* + 10–6 m ouabain; D—15 min with NKR*, 15 min with NKR* + 3.4 x 10–4 m pentobarbital (PB), 15 min with NKR* + PB + ouabain. K influx, net K loss, contraction height, and flow rate were determined, and K efflux was calculated. Decreasing the external calcium concentration ([Ca]e) decreased K efflux with no effect on K influx; restoring [Ca]e increased K efflux without affecting influx. Ouabain decreased K influx more than it decreased K efflux. If [Ca]e was constant, reducing the contraction height with PB did not affect K movements. These findings are consistent with the hypotheses that: 1) calcium and potassium can compete for fixed intracellular anionic binding sites and 2) calcium and ouabain produce their effects on K movements by different means.

scholarly journals Competitive Action of Calcium and Procaine on Lobster Axon

1966 ◽  
Vol 49 (5) ◽  
pp. 1043-1063 ◽  
Author(s):  
Mordecai P. Blaustein ◽  
David E. Goldman
Keyword(s):  
Calcium Concentration ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Giant Axon ◽  
Sodium Conductance ◽  
Potassium Conductances ◽  
Conductance Changes ◽  
Sodium And Potassium ◽  
External Calcium

Voltage clamp studies with the squid giant axon have shown that changes in the external calcium concentration (Frankenhaeuser and Hodgkin, 1957) shift the sodium and potassium conductance versus membrane potential curves along the potential axis. Taylor (1959) found that procaine acts primarily by reducing the sodium and, to a lesser extent, the potassium conductances. Both procaine and increased calcium also delay the turning on of the sodium conductance mechanism. Calcium and procaine have similar effects on lobster giant axon. In addition, we have observed that the magnitude of the response to procaine is influenced by the external calcium concentration. Increasing external calcium tends to reduce the effectiveness of procaine in decreasing sodium conductance. Conversely, procaine is more effective in reducing the membrane conductance if external calcium is decreased. The amplitude of the nerve action potential reflects these conductance changes in that, for example, reductions in amplitude resulting from the addition of procaine to the medium are partially restored by increasing external calcium, as was first noted by Aceves and Machne (1963). These phenomena suggest that calcium and procaine compete with one another with respect to their actions on the membrane conductance mechanism. The fact that procaine and its analogues compete with calcium for binding to phospholipids in vitro (Feinstein, 1964) suggests that the concept of competitive binding to phospholipids may provide a useful model for interpreting these data.

scholarly journals Calcium uptake by mitochondria isolated from muskrat and guinea pig hearts

1991 ◽  
Vol 157 (1) ◽  
pp. 133-142
Author(s):  
T. A. McKean
Keyword(s):  
Guinea Pig ◽  
Calcium Concentration ◽  
Calcium Uptake ◽  
Membrane Damage ◽  
Indirect Measurements ◽  
45Ca Uptake ◽  
Hypoxia Ischemia ◽  
Interfibrillar Mitochondria ◽  
External Calcium

Subsarcolemmal and interfibrillar mitochondria were isolated from the hearts of the diving muskrat and non-diving guinea pig and direct and indirect measurements of calcium uptake were examined in vitro. The calcium-stimulated respiration rate and 45Ca uptake were measured and found to be greater in muskrat than in guinea pig mitochondria. Muskrat mitochondria were able to endure a greater external calcium concentration than guinea pig mitochondria before exhibiting indications of inner membrane damage. Calcium uptake by muskrat heart mitochondria was inhibited more by 1 mmoll-1 MgCl2 than was uptake by guinea pig mitochondria. No differences were detected between the interfibrillar and subsarcolemmal populations of mitochondria within species. An increased ability to sequester calcium by mitochondria without causing them damage may aid an animal during recovery from hypoxia, ischemia or acidosis.

Tension reactivation and potentiation in guinea pig atrium: the effects of isoprenaline, calcium and rate changes

1988 ◽  
Vol 233 (1270) ◽  
pp. 33-43 ◽  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Extracellular Calcium ◽  
Rate Dependence ◽  
Calcium Currents ◽  
Control Medium ◽  
Guinea Pig Atrium ◽  
Guinea Pig Atria ◽  
Degree Of Filling ◽  
Uptake And Release

The process of tension repriming and the phenomenon of tension potentiation after premature stimulation (post-extrasystolic potentiation, PESP) were studied in the adult guinea pig atrium. The following results were obtained. (i) Reducing extracellular calcium, [Ca] o , to 50% of normal did not significantly change the rate of tension repriming. However, in the presence of 5 μm isoprenaline (which greatly speeded up repriming) the same reduction in [Ca] o slowed down the repriming process. (ii) Increases in the rate of stimulation enhanced the rate of tension repriming in a control medium, but this rate-dependence was absent in the presence of isoprenaline. (iii) Isoprenaline (20 μM) abolished PESP. A reduction in [Ca] o or the addition of verapamil (still with isoprenaline) partly restored tension potentiation. In neonatal guinea pig atria, a large PESP was evident, which was only slightly reduced by isoprenaline. These results are interpreted as reflecting changes induced by isoprenaline in the degree of filling of sarcoplasmic reticulum (SR) stores with calcium, and in the rate of calcium recycling between uptake and release sites within the SR network. The large PESP found in the neonate, and its relative insensitivity to isoprenaline was interpreted as reflecting a scarcity of SR. This implies that tension potentiation may also reflect changes in sarcolemmal calcium currents.

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